Click here for the function of IL5.
Edit this page in Wiki Genes - IL5 or see Wiki Gene.
A first class codes for an IL5-specific chain ( hIL5R alpha). Paper-6921480.
Dominant-negative AP-1 inhibited IL-5 transcription. Paper-13431494.
No close relationships were found among TRF, TA, and hTR expression. Paper-2198643.
Priming of the EOS with IL-5 prevented the inhibitory effect of IL-2. Paper-8766534.
Chromosome mapping of the owl monkey CSF1R and IL5 genes. Paper-7448784.
1. IRF-1 lies between IL-5 and CDC25C and is centromeric to IL-3 and GM-CSF. Paper-7730026.
A putative silencer element in the IL-5 gene recognized by Bcl6. Paper-9503156.
TARC and IL-5-positive cases possessed significantly more eosinophils. Paper-14433984.
Proliferation and interleukin 5 production by CD8hi CD57+ T cells. Paper-14308935.
The peak level of ICAM-1 gene expression was seen 6 h after IL-5 stimulation. Paper-152010.
Numerical assessment of the TRF- NOMO/MP2 and EN is performed for several molecules. Paper-12114113.
Serum IL-5 values were significantly higher in both GD and HT in comparison to controls. Paper-14695258.
DESIGN: Caco-2 cells were cultured with IGF-II and IL-5, TNF-alpha or IL-1beta. Paper-11017887.
Differential responsiveness of the IL-5 and IL-4 genes to transcription factor GATA-3. Paper-1600468.
The higher expression rate of IL-5 in PBC was associated with eosinophil infiltration. Paper-2072260.
0. A major fraction of TRF, TCGF, and GM-CSF activities bound to wheat-germ agglutinin. Paper-4061216.
IL-5 and TBXA2R gene polymorphisms were determined by genotyping by using PCR-RFLP assays. Paper-11238809.
Human recombinant IL-1 and murine recombinant TRF/ IL-5 were used in this study. Paper-5806807.
Furthermore, AG490 inhibited IL-5- mediated c-Myc induction and promoter activity. Paper-13682607.
By contrast IL-5, TGF-beta1 and IFN-gamma mRNA analyses were positive in all four BP cases. Paper-9630008.
Trypsin and elastase induced significant IL-5, IL-6, and RANTES secretion from eosinophils. Paper-13070517.
Tryptase induced IL-5 and IL-6 release, but failed to induce RANTES release. Paper-13070517.
Other basophil agonists are GM-CSF, IL-5, NGF and certain chemokines ( IL-8, MCP-1). Paper-448097.
Furthermore, the IL5BS was required for Bcl6 to repress expression of the IL-5 cDNA. Paper-9503156.
Analysis of polymorphisms in olive pollen allergy: IL13, IL4RA, IL5 and ADRB2 genes. Paper-13638207.
In the absence of IL-5, JAK2 and JAK1 were associated with hIL-5Ralpha and betac, respectively. Paper-1370940.
This clearly indicates that surface expression of PAF-R on eosinophils is enhanced by IL-5. Paper-758111.
Cytokines such as IFN-gamma and IL-5, -6, -10, -12, and -15 were expressed in most cases of PBC. Paper-2072260.
Interleukin-5 priming of human eosinophils alters siglec-8 mediated apoptosis pathways. Paper-12660974.
Interleukin-2 inhibits eosinophil migration but is counteracted by IL-5 priming. Paper-8766534.
CONCLUSIONS: IGF-II promotes Caco-2 growth, an effect enhanced with IL-5, TNF-alpha and IL-1beta. Paper-11017887.
IL-5 priming also accelerated Siglec-8-mediated dissipation of mitochondrial membrane potential. Paper-12660974.
Also, in Th2 cells, antisense GATA-3 RNA inhibits IL-5 but not IL-4 promoter activation. Paper-1600468.
Recruitment of histone deacetylase 4 by transcription factors represses interleukin-5 transcription. Paper-12324719.
For eosinophils from allergic subjects, IL-5 also inhibited Mn(2+)- induced adhesion to VCAM-1. Paper-454262.
Association of syntenin with IL-5Ralpha was required for IL-5- mediated activation of Sox4. Paper-9042913.
IFN-alpha inhibited gene expression of IL-5, GM-CSF, TNF-alpha, and IL-13 in PBMC. Paper-905627.
IL-5 rather than eotaxin is effectively decreased by the inhibitory effect of steroid in acute exacerbation. Paper-9819737.
Thus, the histone acetyltransferase (HAT) activity of CBP/p300 was required to activate IL-5 expression. Paper-10468716.
Thus, the IL5BS may act as a silencer element for Bcl6 to repress expression of the IL-5 gene. Paper-9503156.
IL-5 stimulation resulted in tyrosine phosphorylation of JAK2, JAK1, betac, and STAT5. Paper-1370940.
CONCLUSIONS: Pim-1, but not PI3K, plays a major role in IL-5-mediated antiapoptotic signaling in eosinophils. Paper-13662548.
Perilesional skin biopsies from patients with BP were characterized by the deposition of IL-4, IL-13 and IL-5. Paper-8349315.
Association analysis of polymorphisms in IL-3, IL-4, IL-5, IL-9, and IL-13 with Graves' disease. Paper-15178105.
Similarly, serum levels of ECP, IL-5 and IP-10 were significantly higher in acute asthma than in controls. Paper-15146754.
BION-1 blocked eosinophil production, survival, and activation stimulated by IL-5 as well as by GM-CSF and IL-3. Paper-2004650.
These results suggest that IL-5 and TBXA2R genes may be disease-modifying genes in Korean children with atopic asthma. Paper-11238809.
Heterogeneous sandwich assays are demonstrated with parathyroid hormone ( PTH) and interleukin-5 ( IL-5). Paper-8909469.
Interestingly, TARC concentrations in BAL fluids were closely correlated with the concentrations of IL-5 and IL-13. Paper-9204148.
These observations suggest that activation of hIL-5Ralpha-associated JAK2 is indispensable for the IL-5 signaling event. Paper-1370940.
JAK pathway induction of c-Myc critical to IL-5 stimulation of cell proliferation and inhibition of apoptosis. Paper-13682607.
TARC and IL-5 expression correlates with tissue eosinophilia in peripheral T-cell lymphomas. Paper-14433984.
Th2 type cytokines such as interleukin (IL)-4, IL-5, IL-9, and IL-13 are important mediators in allergic inflammation. Paper-10331084.
Interleukin-5 ( IL-5) and eotaxin are directly involved in the airway eosinophilia found in persistent asthma. Paper-9819737.
Furthermore, SHPTP2 appeared to physically associate with beta common (betac) chain of the IL-5 receptor (IL-5betacR). Paper-1130119.
3) The time course of IL-5- induced IL-1 axis molecule expression preceded that of both IL-1beta and IgE immune cxs. Paper-10908094.
The significant positive correlation was found between the activation of AP-1 and the expression of IL-5 mRNA ( P< 0.01). Paper-11533439.
In fact, IL-4 significantly suppressed the antibody response obtained when either IL-2 or BCGFlow was used as a TRF. Paper-7149781.
Proteinase activated receptor-2 mediated IL-5, IL-6 and RANTES release from human eosinophils. Paper-13070517.
CBCL and TRF appeared to screen externalizing and ADHD problems better, while YSR screened internalizing problems better. Paper-12193620.
Chromatin immunoprecipitation showed increased binding of Ets1 and GATA-3 to the IL-5 promoter after stimulation. Paper-13431494.
We found that IL-5 produced a rapid activation and tyrosine phosphorylation of SHPTP2 within 1 min. Paper-1130119.
Steroid treatment markedly decreased eosinophil percentages and IL-5 levels within 7 days but did not alter eotaxin levels. Paper-9819737.
The pathogenesis of nasal polyposis by immunoglobulin E and interleukin-5 is completed by transforming growth factor-beta1. Paper-9774859.
This hypothesis suggests a structural explanation for the 1:1 stoichiometry observed for the complex of hIL-5 with hIL-5R alpha. Paper-418916.
The binding of JAK1 and JAK2 to each hIL-5R subunit was also evaluated in the hIL-5-responsive cell line, TF-h5Ralpha. Paper-1370940.
IL-5- mediated eosinophil survival requires inhibition of GSK-3 and correlates with beta-catenin relocalization. Paper-12131587.
Our results show that children with mycoplasma pneumonia and wheeze have significantly higher serum levels of IL-5 and VEGF. Paper-13737129.
Charcot-Leyden crystal protein was diffusely present in the nucleus and cytoplasm of IL-5-stimulated mature eosinophils. Paper-7337994.
IL-5, eotaxin-1/ CCL11, and eotaxin-3/ CCL26 gene expression levels were measured by real-time PCR. Paper-13028633.
The tyrosine phosphorylated SHPTP2 was complexed with the adapter protein Grb2 in IL-5-stimulated eosinophils. Paper-1130119.
CONCLUSION: Ets1, GATA-3 and AP-1 synergize to regulate IL-5 transcription in human T cells. Paper-13431494.
Salmeterol, but not salbutamol, inhibited IL-5 and IL-13 and enhanced IL-10 synthesis in these cultures. Paper-11168249.
Eosinophils spontaneously released VEGF protein in culture medium, and this release was upregulated by GM-CSF or IL-5. Paper-1089200.
The relationship between IL-5 and TBXA2R gene polymorphisms and pulmonary function in children with asthma has rarely been examined. Paper-11238809.
Neutralization of IFN-gamma resulted in a comparable increase in SWAP-specific IL-10 and IL-5, while IL-4 was not affected. Paper-1869484.
Detailed analysis of the IL-5- IL-5R alpha interaction: characterization of crucial residues on the ligand and the receptor. Paper-309890.
Transactivation by GATA-3 and synergy between GATA-3, Ets1 and AP-1 were verified measuring IL-5 mRNA levels. Paper-13431494.
Terminal eosinophil differentiation is induced by interleukin-5 ( IL-5), which has also been demonstrated to activate STAT5. Paper-9787329.
Cotransfection experiments revealed that both hGATA-4 and PMA/ A23187 stimulation are necessary for the IL-5 promoter activation. Paper-1088999.
The receptors for GM-CSF, IL-3, and IL-5 each possess a cytokine specific alpha subunit, but all three share a common beta chain. Paper-352871.
IL-4, IL-5, TGF-beta1 and IFN-gamma mRNAs detected by a new in situ amplification system in cicatricial pemphigoid. Paper-9630008.
Complicated plaques secreted higher levels of IP-10 (p = 0.027) and lower levels of IL-5 (p = 0.045) than did uncomplicated ones. Paper-15434178.
HCAEC expressed transcripts for interleukin 5 ( IL-5), IL-6, IL-8, and monocyte chemotactic protein-1 ( MCP-1) constitutively. Paper-1689972.
CONCLUSION: Alterations of MMP-2 and -9 expression may play a role in ECRS, but the association with IL-5 and IL-13 remains unclear. Paper-12913573.
Angioedema associated with eosinophilia is not so rare, and IL-5 and VEGF are involved in the pathogenesis of this disease. Paper-11044443.
IL-8 and IL-5 may play crucial roles in recruitment and activation of neutrophils and eosinophils in upper airways of CF patients. Paper-10680608.
Treatment of microglia with IL-5 resulted in the induction of proliferation at levels similar to those induced by GM-CSF. Paper-8886575.
Serum levels of IL-5 and GRO/KC ( IL-8) may be predictive of the inhibitory effect of chemopreventive agents on rat esophageal carcinogenesis. Paper-15113516.
We discuss these findings with regard to the stoichiometry, activation, and signalling of the normal GM-CSF/ IL-3/ IL-5 receptor complexes. Paper-2174016.
CONCLUSIONS: We have demonstrated that in AR, cytokine receptors for IL-4, IL-5, and IFN-gamma follow a similar pattern to their ligands. Paper-1817702.
CONCLUSIONS: We have demonstrated that in AR, cytokine receptors for IL-4, IL-5, and IFN-gamma follow a similar pattern to their ligands. Paper-1595503.
Chromosome 5q candidate genes in coeliac disease: genetic variation at IL4, IL5, IL9, IL13, IL17B and NR3C1. Paper-11160828.
The effect of IL-5 may be that of a cofactor to the chemotactic molecules, of which RANTES may be one of the most important in allergic asthma. Paper-541955.
We have shown that dynamin-2 interacts with the IL-5 receptor-associated tyrosine kinases, Lyn and JAK2, in eosinophils. Paper-12004932.
In contrast to neutrophils, the nuclear segmentation of eosinophils was not induced after incubation with G-CSF, GM-CSF, or IL-5. Paper-6927430.
The LOD was 0.12 microg/l, 0.0077 microg/l, 0.0069 microg/l and 0.0063 microg/l for IL-4, IL-5, IFN-gamma and TNF-alpha, respectively. Paper-9597503.
JAK inhibitor AG490 and c-Myc inhibitor 10058-F4, both, reduced IL-5-mediated cell proliferation in a dose- and time-dependent manner. Paper-13682607.
Conversely, short hairpin RNA-mediated knockdown of RE-IIBP reduces histone H3-K27 methylation and HDAC occupancy around the IL-5 promoter. Paper-14287933.
The hypothesis that IL-2 may be acting via release of interleukin-5 ( IL-5) was tested using an antibody to IL-5 (TRFK-5; 1 mg/kg). Paper-326858.
Cyclic AMP-induced chromatin changes support the NFATc- mediated recruitment of GATA-3 to the interleukin 5 promoter. Paper-13067178.
After 8-72 hours incubation with 0.2-0.4 ng/ml IL-5 or 3-6 ng/ml IL-13, the expression of the MMP-2 and -9 in the CRS cultures was analysed. Paper-12913573.
IFN-gamma also induced Fc gamma RIII expression on peripheral eosinophils but not on eosinophils grown in the presence of IL-5. Paper-8140922.
Interleukin-5 ( IL-5) induction of c-Myc expression is associated with IL-5 inhibition of apoptosis in hematopoietic cells. Paper-13682607.
Several lines of data suggest that the enhanced expression of PAF-R on eosinophils due to IL-5 is the cause of the augmented response to PAF. Paper-758111.
These results suggest that IL5 rs2069812 and IL7R rs1389832, rs1494556 and rs1494555 polymorphisms may contribute to gastric cancer etiology. Paper-12928203.
Eosinophils from asthmatics release IL-5 in an autocrine fashion to prevent apoptosis through upregulation of Bcl-2 expression. Paper-11140549.
A combination of both IL-5 and IL-6 had no additional effect on the enhanced IgA levels than that seen with IL-5 or IL-6 alone. Paper-7358117.
Expression of matrix metalloproteinase-1 mRNA related to eosinophilia and interleukin-5 gene expression in head and neck tumour tissue. Paper-1305171.
Co-incubation with IGF-II and IL-5 increased absorption by 42% (p < 0.001) compared to controls and 18% (p < 0.03) compared to IGF-II alone. Paper-11017887.
IFN-gamma inhibited early progenitor cell division, IL-4 down-regulated early Kit expression, and IL-5 blocked later cell division. Paper-10742071.
Identification of IP-10 and IL-5 as proteins differentially expressed in human complicated and uncomplicated carotid atherosclerotic plaques. Paper-15434178.
CD4 T-lymphocyte activation in asthma is accompanied by increased serum concentrations of interleukin-5. Effect of glucocorticoid therapy. Paper-7584014.
The PPARgamma agonist troglitazone reduced the IL-5-stimulated, but not spontaneous, eosinophil survival in a concentration-dependent manner. Paper-9950152.
Neutralizing antibodies to IL-2, IL-5 and IL-8, leukemia inhibitory factor, and to RANTES were added to the bronchoalveolar lavage fluid. Paper-541955.
Interleukin-5 potentiates the growth response of Caco-2 cells to IGF-II: a role in colonic carcinogenesis complicating ulcerative colitis? Paper-11017887.
A human high affinity interleukin-5 receptor ( IL5R) is composed of an IL5-specific alpha chain and a beta chain shared with the receptor for GM-CSF. Paper-6921480.
We evaluated the serum concentration of interleukin 5 ( IL-5) and the plasma concentration of vascular endothelial growth factor ( VEGF) in 1 patient. Paper-11044443.
Mcl-1 is a common target of stem cell factor and interleukin-5 for apoptosis prevention activity via MEK/ MAPK and PI-3K/Akt pathways. Paper-8380375.
Addition of anti-IL-1 antibody, but not anti- TRF/ IL-5 antibody or anti-IL-2 receptor antibody, inhibited IL-1-induced anti-SRBC responses. Paper-5806807.
Both the PTH assay and IL-5 assays were carried out on microliter volumes and demonstrated physiologically relevant sensitivity (approximately microg/L). Paper-8909469.
Eosinophils were challenged for 16h with different PAR-2 agonists and IL-5, IL-6, and RANTES were measured by a Microplate Reader. Paper-13070517.
Alterations in eotaxin, monocyte chemoattractant protein-4, interleukin-5, and interleukin-13 after systemic steroid treatment for nasal polyps. Paper-10653205.
By mutation studies, it could be shown that Ets1 and Ets2 exerted their effects on the IL-5 promoter through a GGAA motif within the Cle0 element. Paper-1847898.
Effects of G-CSF, GM-CSF, and IL-5 on nuclear segmentation of neutrophils and eosinophils in congenital or acquired Pelger-Huët anomaly. Paper-6927430.
In this study, IL-3, IL-5, and GM-CSF were detected by immunohistochemistry in all patients with CD and DH but not in the control group. Paper-1511884.
The nucleo-cytoplasmic shuttling of HDAC4 was shown to play an important role in the suppressive function of HDAC4 in IL-5 gene expression. Paper-12324719.
EDN release, which ultimately depends on calcium, was inhibited about 30% with PAF, IL5 and sIgA stimulation for normal and atopic donor eosinophils. Paper-13769719.
Cotransfection experiments revealed that both hGATA-4 and phorbol-12-myristate-13-acetate (PMA)-A23187 stimulation are necessary for IL-5 promoter activation. Paper-268120.
Regulation of the human interleukin-5 promoter by Ets transcription factors. Ets1 and Ets2, but not Elf-1, cooperate with GATA3 and HTLV-I Tax1. Paper-1847898.
IL-5 caused translocation of PKCdelta from the cytosol to cell membrane; inhibition of PI3K by wortmannin blocked translocation of PKCdelta. Paper-10774384.
The effect of IL-5 was dose- and time-dependent, with a maximal enhancement of ECP and EPX release of 71% ( P < 0.03) and 66% ( P < 0.03), respectively. Paper-7628016.
Cassette mutagenesis was used to identify side chains in human interleukin 5 ( hIL-5) that mediate binding to hIL-5 receptor alpha chain ( hIL-5R alpha). Paper-418916.
Clonal differences in response to T cell replacing factor ( TRF) for IgM secretion and TRF receptors in a human B lymphoblast cell line. Paper-4247994.
Human interleukin-5 expression is synergistically regulated by histone acetyltransferase CBP/p300 and transcription factors C/EBP, NF-AT and AP-1. Paper-10468716.
AS101 inhibited the production of IL-2R, IL-5 and IL-10 and induced a significant increase in IL-2 levels in the mycosis fungoides PBMCs. Paper-9142981.
Role of activator protein-1 in the transcription of interleukin-5 gene regulated by protein kinase C signal in asthmatic human T lymphocytes. Paper-11533439.
We found that phosphorylation of beta c and JAK2 in response to GM-CSF and IL-5 could be markedly enhanced by depriving cells of endogenous GM-CSF. Paper-1181193.
Treatment with topical steroids downregulates IL-5, eotaxin-1/ CCL11, and eotaxin-3/ CCL26 gene expression in eosinophilic esophagitis. Paper-13028633.
Analysis of 378 cases and 435 age- and sex-matched controls revealed associations for polymorphisms in the Th1 IL7R gene and one polymorphism in the Th2 IL5 gene. Paper-12928203.
Conversely, Th2 cells secrete IL-4, IL-5, IL-9, IL-10, and IL-13 and stimulate type 2 immunity, which is characterized by high antibody titers. Paper-8505061.
Apoptosis in human eosinophils. Programmed cell death in the eosinophil leads to phagocytosis by macrophages and is modulated by IL-5. Paper-7392533.
Dimeric RFX proteins contribute to the activity and lineage specificity of the interleukin-5 receptor alpha promoter through activation and repression domains. Paper-1867040.
Repression of interleukin-5 transcription by the glucocorticoid receptor targets GATA3 signaling and involves histone deacetylase recruitment. Paper-10796566.
Moreover, IL-5- induced dimerization of IL-5R subunits caused JAK2 activation and betac phosphorylation even in the absence of JAK1 activation. Paper-1370940.
The induction of IL-5 gene expression by GATA-3 involves high affinity binding of GATA-3 to an inverted GATA repeat in the IL-5 promoter. Paper-1600468.
Neuraminidase treatment of both hybridoma 123 and spleen cell-derived material resulted in a major peak of each activity ( TRF/ TCGF pI, 4.9; GM-CSF pI, 4.7). Paper-4061216.
Recent studies also indicate that IL-5 and eotaxin, through eosinophils, may regulate Th2 cell function and IL-13 production from this lymphocyte. Paper-10127673.
Eosinophilia was not associated with significant changes in the IL-5 concentration in BAL or the pattern of IL-5 expression in BAL cells. Paper-2011871.
Practical measuring ranges of the non-competitive assays were 100 pg/ml-10 ng/ml for IL-1 beta and TNF alpha and 10 pg/ml 5 for IL-6 and IL-5. Paper-427793.
Background activity of IL-5, Epo, tumor necrosis factor ( TNF), IL-6, or leptin on cells that did not carry the receptor chimeras was very low. Paper-2129260.
Identification of Pim-1 and SLP-76 as regulated by IL-5 led us to suggest a direct role for these proteins in the IL-5 signaling pathway in eosinophils. Paper-9105212.
The major T cell subset involved appears to be the so-called CD4+ Th2 subset which produces interleukin-4 ( IL-4) and interleukin-5 ( IL-5). Paper-707968.
Kinetic studies revealed that IL-1 acts on B cells for the first 2 days and TRF/ IL-5 for the last 3 days in 5-day cultures of B cells. Paper-5806807.
This study presents a formulation of TRF- NOMO second-order Moller-Plesset (MP2) perturbation and Epstein-Nesbet (EN) theory with the use of the TRF Hamiltonian. Paper-12114113.
Comparative cytokine profile of human skin mast cells from two compartments--strong resemblance with monocytes at baseline but induction of IL-5 by IL-4 priming. Paper-10367379.
Moreover, anti- G-CSF, anti- TNF-alpha, anti-GM-CSF, anti-IL-3, and anti- IL-5 antibodies did not suppress the effect of HIL-3 sup on the differentiation of EoL-1 cells. Paper-6904099.
In BALF, TNF-alpha and IL-5 were detected in 2 of 3 and 1 of 3 patients, respectively; however, neither IL-1 beta, GM-CSF, nor IL-3 was detected in any. Paper-1815083.
Of the GATA-binding proteins, only GATA-4 selectively regulates the human IL-5 gene promoter in IL-5 producing cells which express multiple GATA-binding proteins. Paper-1088999.
It was concluded that AP-1 might participate in the signal transduction of PKC- triggered transcription of IL-5 gene in asthmatic T lymphocytes. Paper-11533439.
Results: The serum levels of ECP, IL-5, -6, -8 and -10, G-CSF, MCP-1, IL-1 ra and IP-10 were significantly elevated in acute compared with stable asthma. Paper-15146754.
A serial examination showed that elevated TARC in BAL fluid rapidly fell to below detectable limits preceding decreases in IL-5 concentration and eosinophil percentage. Paper-9204148.
HIL-3 cells express messenger RNA (mRNA) of interleukin-5 ( IL-5), macrophage colony-stimulating factor ( M-CSF), and IL-3 but not granulocyte CSF ( G-CSF). Paper-6904099.
RESULTS: After 72 hours incubation with IL-5, the relative levels of MMP-2 showed no significant alteration in protein expression in comparison with the control groups. Paper-12913573.
Mutation of reporter gene plasmids showed the Ets/NFAT site was of equal importance to the AP-1 and GATA-3 sites in regulating IL-5 transcription. Paper-13431494.
IL-5 and GM-CSF can induce local activation of eosinophils, and IL-1 beta and IL-6 are known to promote T-cell activation and proliferation. Paper-7276981.
This article will detail some of the pathogenic effects regulated by IL-13, IL-5 and the eotaxin subfamily of chemokines to regulate certain aspects of allergic disease. Paper-10127673.
In addition, IFNalpha inhibited the release of eosinophil granule proteins such as eosinophil cationic protein ( ECP), neurotoxin (EDN, or interleukin-5 ( IL-5). Paper-547124.
In addition, cyclic AMP signals enhance histone H3 acetylation at the IL-5 promoter and the concerted binding of GATA-3 and NFATc to the promoter. Paper-13067178.
Inhibition of dynamin by a dominant-negative mutant or by small interfering RNA results in enhancement of IL-5- stimulated ERK1/2 signaling and cell proliferation. Paper-12004932.
The concentrations of IL-4, GM-CSF, and IL-5 in sera from patients with Kimura's disease were within normal ranges or below the detectable level in all sera examined. Paper-13123056.
Culture with GM-CSF induced the binding of radiolabeled IL-5 to EoL-3 cells, with an increased affinity after incubation with IL-3, GM-CSF and IL-5. Paper-7265811.
There were significant differences in CCL5, CCL11, and IL-5 levels of BAL fluid between patients with PF and controls (p < 0.0001, p < 0.0001, and p = 0.001, respectively). Paper-12604028.
In addition to the JAK-STAT and Btk pathway, the Ras- extracellular signal-regulated kinase ( ERK) signals are important for IL-5-dependent cell survival. Paper-12851138.
These data demonstrate that IL-5 priming enhances Siglec-8-mediated mitochondrial and ROS-dependent eosinophil apoptosis and eliminates caspase dependence. Paper-12660974.
No conclusive separation of TRF and TCGF activities was observed in these experiments although GM-CSF differed from TRF and TCGF in that it bound to Concanavalin A. Paper-4061216.
Serum levels of interleukin (IL)-4, IL-5, interferon (IFN)-gamma, and vascular endothelial growth factor ( VEGF) were measured using an enzyme-linked immunosorbent assay kits. Paper-13737129.
The specific binding of [3H]WEB 2086, a specific ligand for PAF-R, to eosinophils treated with 5 ng/ml of IL-5 for 12 h was significantly higher than that to untreated cells. Paper-758111.
The translation- and rotation-free nuclear orbital plus molecular orbital ( TRF- NOMO) theory was developed to determine the nonadiabatic nuclear and electronic wave functions. Paper-12114113.
Neither IL-6 nor anti- IL-6 antibody had any consistent effect on specific antibody production by purified B cells stimulated with antigen and TRF. Paper-7687756.
JAK2 and JAK1 constitutively associate with an interleukin-5 ( IL-5) receptor alpha and betac subunit, respectively, and are activated upon IL-5 stimulation. Paper-1370940.
Interleukin-5 upregulates intercellular adhesion molecule-1 gene expression in the nasal mucosa in nasal allergy but not in nonallergic rhinitis. Paper-152010.
We have previously shown that the transcription factor GATA-3 is expressed in Th2 but not Th1 cells and is crucial for activation of the IL-5 promoter by different stimuli. Paper-1600468.
The spleen cell-derived TCGF and TRF activities focused with isoelectric points (pI) between 3.5 and 6.5 whereas the range for GM-CSF activity was broader (pI, 3.5 to 8.0). Paper-4061216.
Chemotactic responses of eosinophils from patients with allergic rhinitis to 5 STO-2-derived eosinophil chemotactic factors (ECF), IL-3, IL-5 and GM-CSF were examined. Paper-8083097.
Production of IL-2, interleukin-4 ( IL-4) and interleukin-5 ( IL-5) from human peripheral blood mononuclear cells was suppressed by YM-53792 in a dose-dependent fashion. Paper-1231007.
In a murine model of asthma, pretreatment with soluble ST2 reduced production of IL-4, IL-5, and IL-13 from IL-33-stimulated splenocytes. Paper-13417814.
Blockade of adhesion to IL-1-stimulated HUVEC caused by the anti- CD49d monoclonal antibody (MoAb), HP2/1, was comparable for cells cultured with IL-5 and without IL-5. Paper-760610.
The IL-5 augmented the immunoglobulin (Ig) generation of Staphylococcus aureus Cowan strain I (SAC)- activated B blasts in the presence of interleukin-2 ( IL-2). Paper-7721845.
GR recruitment had a profound effect upon the activation capacity of GATA3, which has a binding site close to the NF-AT.AP-1 domain in both IL-5 and IL-13 promoters. Paper-10796566.
This cell line exhibits a dependency on granulocyte-macrophage colony-stimulating factor ( GM-CSF) or interleukin-3 ( IL-3) and responds to interleukin-5 ( IL-5). Paper-8405221.
However, the individual analysis of IL-5, CCL11, and CCL26 expression data suggests that several cytokines and chemokines could participate in the physiopathology of EE in humans. Paper-13028633.
Mean expression levels of eotaxins 1 and 2, IL-5, and CCR-3 were also significantly increased in the patients with eosinophilic esophagitis, albeit at lower levels than eotaxin-3. Paper-12630720.
In contrast, Th2 cells respond to interleukin-4 ( IL-4) to secrete IL-4, interleukin-13 ( IL-13), interleukin-5 ( IL-5), and interleukin-10 ( IL-10). Paper-11227296.
Interleukin-1 beta, interleukin-5, interleukin-6, interleukin-8, and tumor necrosis factor-alpha in chronic sinusitis: response to systemic corticosteroids. Paper-8643252.
In myeloid Kasumi cells, Ets1 and Ets2 failed to stimulate IL-5 promoter activity, unless the T-cell specific transcription factor GATA3 was added. Paper-1847898.
The cytokine protein content ( IL-1 beta, IL-3, IL-4, IL-5, IL-6, IL-8, IL-13, GM-CSF, interferon-gamma) of tissue homogenates was measured using ELISA technique. Paper-1755864.
Thirty-two of 47 cases (68%) showed IL-5-positive lymphoma cells while 15/50 (30%) tumors showed variable staining for TARC in scattered non-lymphoid cells with dendritic morphology. Paper-14433984.
Elevated levels of interleukin (IL)-5 and soluble IL-2 receptor were found in the blood, and skin biopsy specimens demonstrated high levels of IL-5 messenger ribonucleic acid (mRNA). Paper-9266495.
Immunohistochemical analysis revealed numerous IL-5-positive eosinophil cells and TGF-beta1 positivity in the lamina propria of polyp samples, but none in control specimens. Paper-9774859.
Reverse transcription-polymerase chain reaction ( RT-PCR) was employed to assess IL-5 mRNA expression, and electrophoretic mobility shift assays (EMSA) for the activation of AP-1. Paper-11533439.
Thus, we have identified specific functions for dynamin in the IL-5 signaling pathway and demonstrated its role in receptor endocytosis and termination of the ERK1/2 signaling pathway. Paper-12004932.
In this report, we describe the cloning of human GATA-4 ( hGATA-4) and show that hGATA-4 selectively interacts with the -70 GATA site within the IL-5 proximal promoter region. Paper-268120.
In this report, we describe the cloning of human GATA-4 ( hGATA-4) and show that hGATA-4 selectively interacts with the -70 GATA site within the IL-5 proximal promoter region. Paper-1088999.
Of the GATA-binding proteins, only GATA-4 selectively regulates the human interleukin-5 gene promoter in interleukin-5-producing cells which express multiple GATA-binding proteins. Paper-268120.
These results demonstrate the selective role of GATA-4 in the transcriptional regulation of the IL-5 gene in a circumstance where multiple members of the GATA-binding proteins are expressed. Paper-268120.
CONCLUSIONS: The study found increased levels of IL-5 and reduction in ratios of CD4/CD8 lymphocytes in the peripheral blood of patients with HT, but only IL-5 was increased in GD. Paper-14695258.
CONCLUSIONS: Treatment with IQ or ML stimulates the production of GM-CSF, IL-5 and IFNgamma by PBMC, and this is accompanied by an increase of eosinophil- and granulocyte-counts. Paper-11016156.
Relationship between eosinophilia and levels of chemokines ( CCL5 and CCL11) and IL-5 in bronchoalveolar lavage fluid of patients with mustard gas-induced pulmonary fibrosis. Paper-12604028.
Recombinant human IL-5 was shown to induce ICAM-1 gene expression in the nasal mucosa of patients with nasal allergy, but not in the mucosa of non-allergic patients. Paper-152010.
Inhibition of the 5-lipoxygenase pathway abrogated GM-CSF- mediated upregulation by monocytes of allergen-specific interleukin-5 ( IL-5) and IL-13 cytokine production. Paper-12685544.
RESULTS: Both IL-5 and IL-6 levels in PF specimens with endometriosis tended to be higher than normal, while the same specimens were mostly interleukin-1 beta ( IL-1 beta) negative. Paper-7604645.
The underlying mechanisms may involve IL-10- mediated feedback inhibition of IL-5-dependent eosinophil-induced inflammation, which is a common feature of host antiviral responses in early life. Paper-13584429.
In addition, these costimulatory adhesion pathways regulated reciprocal cytokine secretion patterns for interleukin 5 ( IL-5) and granulocyte/macrophage colony-stimulating factor ( GM-CSF). Paper-140209.
Repeated costimulation of CD4+ memory T cells with LFA-3 led to secretion of high levels of IL-5, while repeated costimulation with ICAM-1 induced high levels of secreted GM-CSF. Paper-140209.
A 91% inhibition of eosinophil ADCC was found after pre-incubation of the sera of IL-2-treated patients with anti- IL-5 but not with anti- GM-CSF or anti- TNF alpha Ab. Paper-7888385.
Preincubation of eosinophils with low concentrations of IL-5 caused significantly increased responses toward PF4 and induced a significant chemotactic response toward FMLP and NAF/IL-8. Paper-7373436.
These results suggest that G-CSF plays some role in the nuclear development of neutrophils, whereas IL-5 may not have such an effect on eosinophil maturation in the individual cases studied. Paper-6927430.
Of note, MC precultured in the presence of IL-4 [alone or plus stem cell factor (SCF)] before anti-IgE stimulation, acquired the ability to produce IL-5, and IL-1beta was concomitantly suppressed. Paper-10367379.
Furthermore, YM-90709 inhibited the IL-5- induced but not GM-CSF- induced tyrosine phosphorylation of Janus kinase 2 ( JAK2) in eosinophilic HL-60 clone 15 cells. Paper-9651745.
By gel filtration the T cell-replacing factor ( TRF) activity is present in the 30-15-kDa fraction of T cell supernatants and is associated to interleukin 2 ( IL2). Paper-5178747.
The pharmacological inhibitors of mitogen-activated protein kinase (MAP kinase) and p38 blocked both eotaxin- and IL-5-induced eosinophil shape change in a dose-dependent manner. Paper-9843793.
In this study, we provide first evidence that SH2 protein tyrosine phosphatase 2 ( SHPTP2) phosphotyrosine phosphatase plays a key role in prevention of eosinophil death by IL-5. Paper-1130119.
Recent results have shown that the functional phenotype of CD8+ T cells can be switched from interferon gamma production to IL-4 and IL-5 production by the presence of IL-4. Paper-707968.
Cell supernatants were assayed for Th1 ( IFN-gamma, IL-2, and IL-12p40), Th2 ( IL-4, IL-5, and IL-10), and innate/proinflammatory ( TNF-alpha, GM-CSF, and IL-6) cytokines. Paper-13800719.
Although we saw no association for IL-5 or IL-13 gene variants and prostate cancer risk, our findings call for further evaluation of IL-4 as a contributor to prostate cancer susceptibility. Paper-15190917.
RESULTS: Theophylline significantly inhibited the eosinophil adhesion induced by formyl-methionyl-leucil-phenylalanine ( FMLP) or interleukine-5 ( IL-5) at a concentration within the therapeutic range. Paper-9728214.
Eosinophils incubated with IL-5 or IL-3 showed diminished respiratory burst and mitogen- activated protein kinase kinase phosphorylation in response to further IL-5 stimulation. Paper-9797806.
These results suggest that IL-5 plays an important role in the induction of selective eosinophilia in humans and that IL-5 is produced from T cells with IL-2 stimulation. Paper-6196770.
OBJECTIVE: Transforming growth factor-beta ( TGF-beta) was the only cytokine we tested that inhibited the prolongation of survival of guinea-pig eosinophils induced by IL-5. Paper-900046.
T-helper 1 (TH1) ( interferon-gamma [ IFN-gamma]) and TH2 ( interleukin-4 [ IL-4] and IL-5) cytokines have been variably reported to alter human mast cell numbers in complex culture systems. Paper-10742071.
OBJECTIVE: To determine whether IL-5 (T-746C) and TBXA2R (T924C) gene polymorphisms are associated with asthma phenotype and pulmonary function in Korean children with atopic and nonatopic asthma. Paper-11238809.
We examined the expression of VEGF messenger RNA (mRNA) and protein by human eosinophils in response to granulocyte-macrophage colony-stimulating factor ( GM-CSF) and interleukin-5 ( IL-5). Paper-1089200.
The effect of interleukin-5 ( IL-5) on intercellular adhesion molecule-1 ( ICAM-1) gene expression in human nasal mucosa was studied using the method of gene expression quantification. Paper-152010.
We propose that the unique regulatory mechanism of IL-5 gene transcription involves the reversible histone modification catalysed by HDAC4 and p300, which are recruited by the transcription factors. Paper-12324719.
Furthermore, a significant increase of antigen-induced production of GM-CSF, IL-5 and IFNgamma by PBMC was observed in the IQ- and ML-group but not in the groups receiving ML-depleted IQ or placebo. Paper-11016156.
When the relative amount of PAF-R mRNA was determined by reverse transcription PCR, the message was found to be increased through activation of transcription of transcript 1 on exposure to IL-5. Paper-758111.
Here, we show that transcriptional repression of the Interleukin-5 gene involves recruitment of GR to a DNA region located within the IL-5 proximal promoter, which is bound by NF-AT and AP-1 proteins. Paper-10796566.
IFN-gamma (100 U/ml) and TNF-alpha (1000 U/ml) or IL-5 (200 pM) caused a significant increase in the expression of the eosinophil peroxidase ( EPO) and the major basic protein (MBP) genes. Paper-10177763.
We detected an increase of BMK13-positive and eotaxin-positive cells in the nasal lamina propria and enhanced expression of IL-5 in the nasal epithelium of atopic subjects only at T(24) (p < 0.05). Paper-8398552.
They also reduced the levels of the serum cytokines, interleukin 5 ( IL-5) and GRO/KC, the rat homologue for human interleukin-8 ( IL-8), and this was associated with increased serum antioxidant capacity. Paper-15113516.
In contrast, stimulation of the cells with granulocyte-macrophage colony-stimulating factor ( GM-CSF) or interleukin-5 ( IL-5) results in maintenance or upregulation of Bcl-xL mRNA and protein levels. Paper-1522989.
Immunoglobulin E (n = 13), IL-5 (n = 22), and TGF-beta1 (n = 27) concentrations were measured with enzyme-linked immunosorbent assay technique in homogenized polyp tissue and in control mucosa. Paper-9774859.
Recently, transforming growth factor-beta ( TGF-beta) has been shown to induce IgA isotype switch at a clonal level and interleukin 5 ( IL5) promotes differentiation into IgA-bearing B cells. Paper-139994.
INTERVENTION: Pulmonary function tests, tests for D(LCO), computed tomography scans of the chest, analyses of BAL fluids for RANTES ( CCL5), eotaxin ( CCL11), and IL-5 were performed in all cases. Paper-12604028.
In vitro, IL-17 reduced TARC production in dendritic cells (DCs)-the major source of TARC-and antigen uptake by DCs and IL-5 and IL-13 production in regional lymph nodes. Paper-12334513.
Tixocortol pivalate (10(-6) to 3 x 10(-5) M) caused a concentration-related inhibition of IL-5 release but only the highest concentration tested inhibited the release of IFNgamma. Paper-1928863.
Western blot analysis demonstrated that extracellular signal-regulated kinase phosphorylation, a critical intermediary in adhesion elicited by IL-5, was blocked by inhibition of either PI3K or PKC-delta. Paper-10774384.
These data suggest that extracellular signal-regulated kinase-mediated adhesion of beta(2)-integrin caused by IL-5 is mediated in human eosinophils by a class IA PI3K through activation of a PKCdelta pathway. Paper-10774384.
First, we demonstrate that IL-5 induced c-Myc RNA and protein expressions, as well as activated Janus kinases ( JAK1 and JAK2) and signal transducer and activator of transcription-5b (STAT5b). Paper-13682607.
A concentration of interleukin-5 ( IL-5) and TNF-alpha in serum was detected in five cases; however IL-1 beta, GM-CSF, and IL-3 were detected in 3 of 5, 2 of 5, and 1 of 5 patients, respectively. Paper-1815083.
Cyclosporin A and rapamycin significantly inhibited IL-5- enhanced ECP release in a concentration-dependent fashion, whereas dexamethasone did not. Paper-1378248.
However, cytokines that prime basophils but do not induce degranulation, such as interleukin-5 ( IL-5) and granulocyte/macrophage colony- stimulating factor ( GM-CSF), have been detected at sites of LPR. Paper-820844.
The comparison between the untreated polyp group and controls showed significantly higher concentrations of IL-5, eotaxin, ECP, and albumin in polyp supernatants, whereas TGF-beta 1 was significantly lower. Paper-8573523.
CONCLUSION: The current study indicates that IL-5 (T-746C) and TBXA2R (T924C) polymorphisms alone are associated with spirometric markers of asthma severity, whereas they are not associated with presence of asthma per se. Paper-11238809.
This study demonstrates that eosinophils from asthmatics release IL-5 in an autocrine fashion to act on their own IL-5 receptors in prevention of apoptosis through the upregulation of Bcl-2 expression. Paper-11140549.
1) Pre-treatment of isolated rabbit tracheal rings with the inhibitory IL-1 axis members, IL-1 receptor antagonist and IL-1 type-II receptor abrogated both IL-5- and IgE cx-induced changes in ASM responsiveness. Paper-10908094.
The ability of CD8hi CD57+ T cells to further differentiate is highlighted by a distinct cytokine profile late after activation that includes the unexpected release of high levels of interleukin 5. Paper-14308935.
When these cytokines were administered to mature mast cells, IFN-gamma and IL-5 had no effect on degranulation and cell division, but IL-4 induced division and potentiated FcepsilonRI-mediated degranulation. Paper-10742071.
Three residues in the common beta chain of the human GM-CSF, IL-3 and IL-5 receptors are essential for GM-CSF and IL-5 but not IL-3 high affinity binding and interact with Glu21 of GM-CSF. Paper-139387.
CBDMC expressed tumor necrosis factor-alpha ( TNF-alpha) and the eosinophil-active growth factors, interleukin-5 ( IL-5) and granulocyte-macrophage colony-stimulating factor ( GM-CSF) after activation. Paper-9649585.
The results suggested that CysLTs stimulate eosinophils to induce TGF-beta1 production in allergic inflammation where IL-5 and GM-CSF are abundant and may be involved in the pathogenesis of airway remodeling. Paper-11251263.
Finally, both the mitochondrial electron transport inhibitor rotenone, and the ROS inhibitors diphenyleneiodonium and antimycin, completely inhibited Siglec-8-mediated apoptosis, even after IL-5 priming. Paper-12660974.
In the chromatin immunoprecipitation assays, we showed that RE-IIBP overexpression induces histone H3-K27 methylation, HDAC recruitment, and histone H3 hypoacetylation on the IL-5 promoter and represses expression. Paper-14287933.
Eosinophil numbers were increased in both mild and severe asthma, but interleukin-5 ( IL-5) levels were highest in mild asthma, whereas eosinophil cationic protein ( ECP) levels were highest in severe asthma. Paper-2039254.
Studying the regulation of IL-5 gene expression by Ets transcription factors, we found that Ets1 and Ets2, but not Elf-1, were able to activate the human IL-5 promoter in Jurkat T-cells. Paper-1847898.
In conclusion, induction of IL-5, IL-6, and RANTES release from eosinophils by trypsin and elastase and IL-5 and IL-6 secretion from eosinophils by tryptase is via activation of PAR-2. Paper-13070517.
Anti-IL-10 also up-regulated SEA-specific IFN-gamma protein and mRNA responses in most splenocyte cultures from hepatosplenic schistosomiasis patients but had no effect on antigen-specific IL-4 or IL-5 production. Paper-1869484.
Specifically, stimulated production of the cytokines interleukin 4 ( IL-4), interleukin-5 ( IL-5), interleukin-13 ( IL-13), interferon-gamma ( IFN-gamma), as well as eosinophil count, was measured. Paper-12024161.
IFN-alpha efficiently used for the treatment of hypereosinophilic syndromes can significantly decrease eosinophil degranulation and IL-5 release by eosinophils, through binding to a receptor for IFN-alpha. Paper-295495.
A total of 62 SNPs were analysed in eight of the 25 genes; ICOS, IL4, IL5, IL13, CSF2, CTLA4, the inducible T-cell tyrosine kinase ( ITK) and CD3D. Paper-14000340.
Our data indicate that IL-5 and TARC expression highly correlate with eosinophilia in T-cell lymphomas, suggesting that these chemokines are involved in the recruitment of eosinophils into the tumors. Paper-14433984.
This is the first report describing a potential role for GSK-3 and beta-catenin in regulating eosinophil survival and suggests a novel mechanism by which IL-5 inhibits the constitutive apoptotic program in these cells. Paper-12131587.
METHODS: Eosinophils in peripheral blood of healthy volunteers were purified and cultured with interleukin-5 ( IL-5), granulocyte/macrophage colony-stimulating factor ( GM-CSF) or interferon-gamma ( IFN-gamma). Paper-2024972.
OBJECTIVES: To determine whether pro-inflammatory cytokines associated with colitis, namely IL-5, TNF-alpha and IL-1beta, alter the proliferative effect of IGF-II on the colorectal cancer cell line, Caco-2. Paper-11017887.
Only SHPTP2 antisense oligonucleotides, but not sense SHPTP2, could inhibit tyrosine phosphorylation of microtubule-associated protein kinase, and reverse the eosinophil survival advantage provided by IL-5. Paper-1130119.
Relative to controls, atopic sensitized ASM cells exhibited an early increased mRNA expression of the TH2-type cytokines, interleukin-5 ( IL-5) and granulocyte-macrophage colony-stimulating factor ( GM-CSF), and their receptors. Paper-1808553.
METHODS: We conducted an association study between known polymorphisms of IL-5 (T-746C) and TBXA2R (T924C) and asthma phenotype and the parameters of atopy and pulmonary function in atopic and nonatopic Korean children with asthma. Paper-11238809.
IL-5 mRNA from peripheral blood mononuclear cells and the colon lesion were detected by the reverse-transcriptase polymerase chain reaction method, indicating that IL-5 can also be of importance in ulcerative colitis. Paper-1632803.
Fanconi anemia (FANC) and pulmonary alveolar proteinosis associated with deficiency of the beta-chain common to the GM-CSF/ IL3/ IL5 receptors (beta c-PAP) are rare inherited disorders of childhood or adolescence. Paper-8326885.
Characterization of the largest element in yeast artificial chromosome transgenic mice revealed it to be a coordinate regulator of three genes, interleukin-4, interleukin-13, and interleukin-5, spread over 120 kilobases. Paper-2162814.
Specificity studies under conditions that prevent receptor internalization showed that the binding of IL-3, GM-CSF, and IL-5 was not inhibited by tumor necrosis factor (TNF)-alpha, IL-1 beta, interferon (IFN)-gamma, or G- CSF. Paper-6629922.
Human interleukin-5 ( IL-5), granulocyte-macrophage colony-stimulating factor ( GM-CSF), and IL-3 are eosinophilopoietic cytokines implicated in allergy in general and in the inflammation of the airways specifically as seen in asthma. Paper-2004650.
The following cytokines were analyzed by cytometric bead array: interleukin 2 ( IL-2), interleukin 4 ( IL-4), interleukin 5 ( IL-5), interleukin 10 ( IL-10), tumor-necrosis-factor α (TNF-α), and interferon γ (INF-γ). Paper-15851850.
Results: Fulminant hepatic failure patients showed a high number of intrahepatic eosinophils concomitant with an increased expression of IL-6, besides the IL-6-positive eosinophils associated with the lack of IL-5. Paper-13686856.
In this study we have focused on analysing the molecules that selectively regulate eosinophil migration, namely eotaxin and interleukin-5 ( IL-5), using an enzyme-linked immunosorbent assay in patients with strongyloidiasis. Paper-12076470.
In a murine myeloid cell line (FDC-P1), transfected with minigenes allowing expression of either IL-5Ralpha variant, IL-5 itself, but not IL-3 or GM-CSF, stimulated a reversible switch toward expression of TM-IL-5Ralpha. Paper-2144149.
These results suggest that IL-5 induces cell proliferation and anti-apoptosis through the JAK/ c-Myc pathway, and that JAK1 and JAK2 activation participate in IL-5- induced up-regulation of c-Myc. Paper-13682607.
A combination of LTD(4) and IL-5 or LTD(4) and GM-CSF synergistically induced TGF-beta1 expression in eosinophils although stimulation with single factor, LTD(4), IL-5 or GM-CSF did not induce the gene expression. Paper-11251263.
The aim of this study is to evaluate the expression of mRNA for IL-4, IL-5, TGF-beta1, IFN-gamma in patients with CP, and investigate the role of the cytokine profile as a possible cause of the clinical features and course of the disease. Paper-9630008.
There is strong evidence that the Chr.5q31-33 region, which contains the immune response cytokine genes [interleukin (IL)-3, IL-4, IL-5, IL-9, and IL-13], is linked to autoimmune thyroid disorders in Chinese and Japanese populations. Paper-15178105.
OBJECTIVE: To determine alterations in Th2 chemokines eotaxin and monocyte chemoattractant protein-4 ( MCP-4), and cytokines interleukin-5 ( IL-5) and interleukin-13 ( IL-13), in nasal polyps (NP) after steroid treatment. Paper-10653205.
Studies of the mechanism of this antagonism showed that BION-1 prevented the high-affinity binding of (125)I- IL-5, (125)I- GM-CSF, and (125)I-IL-3 to purified human eosinophils and that it bound to the major cytokine binding site of beta(c). Paper-2004650.
Regarding alphadbeta2 ligands, in both freshly isolated and IL-5-cultured eosinophils, as well as alphadbeta2-transfected Chinese hamster ovary cells, alphadbeta2 can function as a ligand for vascular cell adhesion molecule 1 ( VCAM-1). Paper-1686667.
IL-3 and GM-CSF also supported eosinophil development and up-regulation of TM-IL-5Ralpha mRNA in this system, but this was preceded by expression of IL-5 mRNA and was inhibited by monoclonal antibody to IL-5. Paper-2144149.
In an attempt to detect genes modulated by one of these factors, cells were infected with the Rosabetageo retrovirus in the presence of GM-CSF, IL-3, or IL-5 and clones were selected for retroviral integration on the basis of G418 resistance. Paper-8405221.
At baseline the two groups did not differ with respect to BAL fluid concentrations of cyclooxygenase products, peptido-leukotrienes, histamine, tryptase, interleukin-5 ( IL-5), eosinophil cationic protein ( ECP), or eosinophil number. Paper-812063.
We examined the effects of IL-12 on the productions of IL-5 and granulocyte/macrophage colony- stimulating factor ( GM-CSF) by antigen ( Dermatophagoides farinae, Df)-stimulated mononuclear cells (MNCs) from asthmatic patients in vitro. Paper-1288834.
Our study identifies IP-10 and IL-5 as proteins differentiating complicated and uncomplicated plaques from human carotid arteries and provides new insights into the interplay of molecular mediators with atherosclerotic plaque progression. Paper-15434178.
The synergism of GATA3 with either Ets1 or Ets2 may play an important role in calcium- or Tax1-dependent regulation of IL-5 expression in Th2 cells or in HTLV-I transformed adult T-cell leukemia cells, respectively. Paper-1847898.
Transgenic mice in which interleukin-5 ( IL-5) expression is driven by a keratin-14 ( K14) promoter had many eosinophils in the epidermis, and the number of nerves was also significantly increased in the epidermis. Paper-16130250.
Peripheral blood eosinophils were cultured with leukotriene D(4) (LTD(4)) and/or interleukin-5 ( IL-5) or granulocyte colony-stimulating factor ( GM-CSF) for 16 h and gene expression of TGF-beta1 was quantified with real-time PCR. Paper-11251263.
Furthermore, in the acute phase, elevated serum levels of ECP, IL-5, IL-6, IL-1 ra and IP-10, but not IL-8, IL-10, G-CSF and MCP-1 were significantly reduced after treatments that included systemic corticosteroids. Paper-15146754.
Since the unidirectional species specificity is due only to the interaction with the IL-5R alpha subunit, we have used chimeric IL-5R alpha molecules to define regions of hIL-5R alpha involved in species-specific hIL-5 ligand binding. Paper-309890.
2fTGH cells, stably transfected with these receptor chimeras, responded to very low concentrations of IL-5 or Epo ( IC50 values of approximately 15 pg and 3 pg/ml, respectively) and thus can be used as a very sensitive bioassay for both ligands. Paper-2129260.
Significant proliferation (SI greater than or equal to 3.0) was induced by interleukin-6 ( IL-6) in six of ten patients (SI of 31 and 43 in two cases); and to interleukin-3 ( IL-3) and interleukin-5 ( IL-5), independently, in two patients each. Paper-6315244.
Because inhibition of NFATc binding to the IL-5 promoter in vivo also affects the binding of GATA-3, one may conclude that upon induction of Th2 effector cells NFATc recruits GATA-3 to Th2-type genes. Paper-13067178.
We have investigated the modulatory role of IL-5 on N-formyl-methionyl-leucyl-phenylalanine ( FMLP), neutrophil-activating factor (NAF/IL-8), platelet factor 4 ( PF4), and cytokine-induced chemotaxis of eosinophils from normal individuals. Paper-7373436.
The authors analyze the possible implication of 7 genetic polymorphisms described as asthma susceptibility genes: IL13 (C-1112T and R130Q), IL4RA (I50V, Q551R), IL5 (C-746T) and ADRB2 (Q27E and R16G) in specific olive pollen allergic sensitization. Paper-13638207.
In the absence of T helper cells antibody responses to influenza virus were completely restored with T cell replacing factor [ TRF; IL-2 or low-molecular-weight B cell growth factor (BCGFlow)], but not with IL-4. Paper-7149781.
In addition, plasma levels were determined in all of the patients for the platelet-derived chemokine beta-thromboglobulin (beta-TG) and for IFN-gamma, interleukin (IL)-2, IL-4, IL-5, and IL-10, along with serum IgE levels and blood eosinophils. Paper-8818585.
Src homology 2 protein tyrosine phosphatase (SHPTP2)/Src homology 2 phosphatase 2 ( SHP2) tyrosine phosphatase is a positive regulator of the interleukin 5 receptor signal transduction pathways leading to the prolongation of eosinophil survival. Paper-1130119.
Addition of a specific TGF-beta 1 antibody reversed the inhibitory effect of some concentrates on IL-2 secretion by PHA- stimulated Jurkat T cells and interleukin-5 (IL-5)-induced proliferation of an erythroleukemic cell line. Paper-131771.
RESULTS: Surface expression of very late antigen-4 [VLA-4] and LFA-1 was decreased and the production of the type 2 cytokines IL-5 and IL-13 was augmented by the presence of IL-4 during stimulation of CD8+ T cells from mild atopic asthmatics. Paper-11243643.
From studies on mouse cells, the activation protein (AP)-1 and GATA-3 sites in the proximal promoter region appear to be important in IL-5 regulation but the significance of an adjacent Ets/nuclear factor of activated T cell (NFAT) site has been less clear. Paper-13431494.
Therefore, we conclude that the physical association of SHPTP2 with the phosphorylated betac receptor and Grb2 and its early activation are required for the coupling of the receptor to the Ras signaling pathway and for prevention of eosinophil death by IL-5. Paper-1130119.
The interleukin 5 ( IL-5) receptor consists of an IL-5-specific alpha-subunit (IL-5Ralpha) and a signal-transducing beta-subunit (betac) shared with the IL-3 and granulocyte-macrophage colony-stimulating factor ( GM-CSF) receptors. Paper-9042913.
In atopic children with asthma, we identified a significant gene-gene interaction in that the combination of the IL-5 (T-746C) and TBXA2R (T924C) mutant alleles was shown to be associated with reduced pulmonary function as determined by FEF 25-75% (%) measurement. Paper-11238809.
IL-1 could induce little, if any, differentiation in antigen-primed B cells, LPS-stimulated B-cell blasts, or BCL1 cells into antibody-secreting cells, whereas differentiation could be induced by low doses of TRF/ IL-5 (1-2 U/ml). Paper-5806807.
PPARalpha was demonstrated, for the first time, to regulate the IL-4 and IL-5 genes and to bind the IL-4 promoter in the presence of steroid receptor coactivator-1, indicating that PPARalpha can directly transactivate the IL-4 gene. Paper-13675099.
Under conditions where Th0 cells are generated, co-culture with anti-CD2 F(ab')2 MoAb led to the generation of Th cells that secreted 30-35% less IL-5, while not affecting secretion of IFN-gamma or granulocyte-macrophage colony-stimulating factor ( GM-CSF). Paper-1469358.
In the present study, we investigated effects of tryptase, trypsin, elastase, and agonist peptides of proteinase activated receptor-2 ( PAR-2) SLIGKV-NH(2) and tc-LIGRLO-NH(2) on IL-5, IL-6 and RANTES release from highly purified human eosinophils. Paper-13070517.
Our results indicate that acquisition of IL-5 secretion capability by Th cells is regulated mainly by signals transduced by the TCR/CD3 complex and by the presence of interleukin-4 ( IL-4), while the CD2/LFA-3 pathway plays an additional, but minor, role. Paper-1469358.
Following anti-parasite therapy, secretion of IL-12p40 and IL-5 augmented significantly in treated patients while IL-10, MDC, MIP-1alpha, TARC and IL-8 substantially diminished (all p<10(-5)) when their PBMC were activated with parasite- and bacteria-specific antigens. Paper-10809444.
These findings suggest that a significant cytotoxicity against tumor cells can be mediated by eosinophils after indirect, IL-5- mediated in vivo activation by IL-2, and that eosinophils may be involved in the anti-tumor response(s) induced in vivo by IL-2. Paper-7888385.
The receptor for interleukin 5 ( IL-5) consists of a cytokine-specific alpha chain (IL-5Ralpha) and a signaling beta chain, which is shared with interleukin 3 ( IL-3) and granulocyte-macrophage colony-stimulating factor ( GM-CSF). Paper-2144149.
The high affinity receptor for IL-5 (IL-5R) is composed of an alpha subunit ( IL-5R alpha) expressed by the eosinophil lineage, that associates with a beta c subunit shared with the receptors for IL-3 and granulocyte-macrophage colony stimulating factor ( GM-CSF). Paper-155642.
When CD4(+) T cells from Bcl6-deficient and lck-Bcl6-transgenic mice were stimulated with anti-CD3 Abs, production of IL-5 among Th2 type cytokines was preferentially affected by the amount of Bcl6 in the T cells. Paper-9503156.
Furthermore, the expression of B-cell lymphoma-2 ( Bcl-2) proteins was significantly inhibited by the anti- hIL-5 Ralpha Ab or antisense IL-5 oligonucleotides in asthmatics (p<0.05, n=8), but there was no significant change in eosinophils from normal subjects. Paper-11140549.
In prednisolone-treated patients there was also a reduction in the number of cells expressing mRNA for interleukin-4 ( IL-4, p < 0.01), and interleukin-5 ( IL-5, p < 0.03) and an increase in cells expressing mRNA for interferon-gamma ( IFN-gamma) (p < 0.01). Paper-484168.
RESULTS: Although pharmacologic inhibition of phosphatidylinositol-3 kinase ( PI3K) by LY294002, wortmannin, or the selective PI3K p110delta isoform inhibitor IC87114 was successful in each case, only LY294002 blocked increased IL-5-mediated eosinophil survival. Paper-13662548.
METHODS: Highly purified eosinophils were stimulated for O2- release with platelet-activating factor (PAF) or interleukin-5 ( IL-5), while for EPO release complement fragment (C5a) or N-formyl-methionyl-leucyl-phenylalanine ( FMLP) was employed. Paper-1320216.
We found a putative Bcl6- binding sequence (IL5BS) on the 3' untranslated region in the murine and human IL-5 genes, and specific binding of Bcl6 protein to the sequence was confirmed by gel retardation assay and chromatin immunoprecipitation assay. Paper-9503156.
To activate the IFN signaling pathway, we made receptor chimeras, consisting of the IFN type I receptor intracellular and transmembrane domains, fused to either the interleukin-5 ( IL-5) receptors or erythropoietin ( Epo) receptor extracellular domains as model systems. Paper-2129260.
The concentrations of ECP and cytokines ( interleukin-4 ( IL-4), granulocyte-macrophage colony-stimulating factor ( GM-CSF), and interleukin 5 ( IL-5)) in sera from patients with Kimura's disease were measured by enzyme-linked immunosorbent assay ( ELISA). Paper-13123056.
Concentrations of cytokines ( interleukin-1 beta ( IL-1 beta), tumor necrosis factor-alpha ( TNF-alpha), interleukin-3 ( IL-3), interleukin-5 ( IL-5) and granulocyte/macrophage colony stimulating factor ( GM-CSF) were measured using ELISA. Paper-1815083.
Peak proliferation to IL-5 or IL-6 and to IL-3 occurred in cells pulsed with 3[H] thymidine at 24 and 48 hours, respectively; and proliferation to combinations of factors did not exceed that noted to IL-6 alone; Ig secretion was not documented under any culture conditions. Paper-6315244.
To examine whether endogenously produced GM-CSF activates intracellular GM-CSF/IL-3/ IL-5-related signal transduction pathways, we performed antiphosphotyrosine immunoblotting of cell lysates of AML14.3D10 cells before and after deprivation of endogenous GM-CSF. Paper-1181193.
Identification of a 14-3-3 binding sequence in the common beta chain of the granulocyte-macrophage colony-stimulating factor ( GM-CSF), interleukin-3 ( IL-3), and IL-5 receptors that is serine- phosphorylated by GM-CSF. Paper-2004649.
Although incubation of eosinophils in culture medium reduced steady-state VEGF mRNA levels, eosinophil VEGF mRNA levels were enhanced by GM-CSF and IL-5, and this enhancement was blocked by the transcription inhibitor actinomycin D. Paper-1089200.
Expression of CD25, human lymphocyte antigen (HLA-)DR, CD45RA, and CD45RO on CD4 and CD8 T lymphocytes was measured by flow cytometry, and serum concentrations of interleukin-5 ( IL-5) were measured using an enzyme-linked immunosorbent assay technique. Paper-7584014.
ASA airways demonstrated a significant 2-fold increase in the total number of submucosal inflammatory cells expressing IL-5 (p = 0.03) and approximate 4- and 2-fold increases in the numbers of mast cells expressing IL-5 and GM-CSF (p = 0.02 and p = 0.04, respectively). Paper-1238812.
We evaluated the safety and pharmacokinetics of reslizumab, and biologic activity was assessed by means of endoscopic evaluation of polyp size, symptoms, peripheral eosinophil counts, peripheral and local IL-5 levels, eotaxin levels, and eosinophil cationic protein levels. Paper-12304992.
Exposure of PMN and MN cells to the leukocyte-activating cytokines interleukin (IL)-3, IL-5, and granulocyte-macrophage colony-stimulating factor resulted in a several-fold increase of TGF-alpha mRNA expression and protein release by eosinophils, but not by neutrophils and MN cells. Paper-7937824.
Comparable effects were obtained with eosinophils cultured with interleukin 5 ( IL-5), granulocyte-macrophage colony-stimulating factor ( GM-CSF) and, to a lesser extent, by tumor necrosis factor-alpha ( TNF alpha), while no direct activity was mediated by IL-2. Paper-7888385.
We have examined the repeatability and the validity of an improved method to measure sputum cells and fluid-phase eosinophil cationic protein ( ECP), major basic protein (MBP), eosinophil-derived neurotoxin ( EDN), albumin, fibrinogen, tryptase, and interleukin-5 ( IL-5). Paper-679570.
This eosinophil viability-sustaining activity was inhibited by 76 +/- 7% (mean +/- SEM; n = 3) by the addition of anti- interleukin 5 ( IL-5) but not by neutralizing antibodies monospecific for either granulocyte/macrophage colony- stimulating factor ( GM-CSF) or IL-3. Paper-6749266.
We provide evidence that HDAC4 ( histone deacetylase 4) and p300, a known HAT (histone acetyltransferase), reversibly controlled the activity of the IL-5 promoter in vivo and in vitro, with a concurrent alteration of histone H3 acetylation status at the promoter regions. Paper-12324719.
METHODS: We investigated the relationship of polymorphisms in interleukin 4 ( IL4), IL5, IL10, IL13, and transforming growth factor (TGFbeta1) with spontaneous preterm birth and small-for-gestational age (SGA) in a nested case-control study of a prospective pregnancy cohort. Paper-11134721.
We conclude that PBMC of patients with acute exacerbations of asthma demonstrate elevated expression of mRNA encoding IL-5, but not IL-2, IL-4 and IFN gamma and that the clinical improvement associated with glucocorticoid therapy is associated with a reduction of IL-5 mRNA expression. Paper-148226.
We have assayed genetic variation at the IL4, IL5, IL9, IL13, IL17B and NR3C1 ( GR) loci, all of which are present on chromosome 5q and have potential or demonstrated involvement in autoimmune and/or inflammatory disease, in a sample of 409 CD cases and 355 controls. Paper-11160828.
The common beta chain (beta(c)) of the granulocyte-macrophage colony-stimulating factor ( GM-CSF), interleukin-3 ( IL-3), and IL-5 receptors is the major signaling subunit of these receptors coupling ligand binding to multiple biological activities. Paper-2004649.
Five related cytokine genes, interleukin 3 ( Il3), interleukin 4 ( Il4), interleukin 5 ( Il5), interleukin 13 ( Il13), and granulocyte-macrophage colony-stimulating factor (Csfgm or Csf2), are tightly linked on mouse chromosome 11. Paper-8393568.
HEL and cytokine ( interleukin-4 ( IL-4), interleukin-5 ( IL-5), interleukin-10 ( IL-10), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ)) levels were measured by enzyme-linked immunosorbent assay ( ELISA) from tear samples of AKC patients and control subjects. Paper-15544345.
Expression of the beta 2 integrins (CD11/CD18) and the beta 1 integrin, VLA-4 ( CD49d/ CD29), was assessed during development in culture with IL-3, IL-5, and granulocyte-macrophage colony stimulating factor in cultures of human umbilical cord blood-derived eosinophil (CDE) precursor cells. Paper-760610.
Viability of eosinophils was counted and supernatants were tested for the presence of cytokines by neutralization of eosinophil viability-enhancing activity with specific antibodies to IFN-gamma, interleukin-5 ( IL-5), IL-3, or granulocyte-macrophage colony-stimulating factor ( GM-CSF). Paper-8083104.
Using IL-5 as the priming stimulus, the rate of Siglec-8-induced eosinophil apoptosis was found to be enhanced compared with unprimed cells, and mechanisms differed after IL-5 priming in that neither a pan-caspase inhibitor, nor a specific caspase-3 inhibitor, could override apoptosis. Paper-12660974.
CONCLUSION: Overall our data shows that CT IncB and IncC are able to upregulate expression of cytokines, namely interferon-gamma, IL-12, IL-23 and GM-CSF in CT-positive fertile women while expression of IL-1 Beta, IL-4, IL-5, IL-6 and IL-10 were upregulated in CT-positive infertile women. Paper-13972544.
Eosinophil survival-promoting cytokines such as interleukin 5 ( IL-5) and granulocyte-macrophage colony-stimulating factor ( GM-CSF) failed to block apoptosis and instead enhanced the sensitivity of eosinophils to undergo apoptosis in response to Siglec-8 antibody. Paper-9899269.
Accordingly, we provide evidence that cytokines regulating eosinophils proliferation and activation, ie, interleukin-5 ( IL-5), IL-3, and granulocyte-macrophage colony-stimulating factor ( GM-CSF), are able to enhance the cellular density of CD30L on purified eosinophils from normal subjects. Paper-760588.
Differential regulation of human eosinophil IL-3, IL-5, and GM-CSF receptor alpha-chain expression by cytokines: IL-3, IL-5, and GM-CSF down-regulate IL-5 receptor alpha expression with loss of IL-5 responsiveness, but up-regulate IL-3 receptor alpha expression. Paper-9797806.
Serial nasal lavage samples were analyzed for the presence of inflammatory cells ( eosinophils and neutrophils) and soluble markers associated with cellular inflammation [ interleukin-5 ( IL-5), interleukin-8 ( IL-8), eosinophil cationic protein ( ECP) and myeloperoxidase ( MPO)]. Paper-9696434.
Addition of IL-1 to the culture of normal B-cells and sheep red blood cells (SRBC) induced a dose-dependent anti-SRBC IgM response, with maximal response at 100 U/ml, whereas the response induced by TRF/ IL-5 was less than that induced by IL-1 and did not reach the maximum even at 100 U/ml. Paper-5806807.
RESULTS: Significant higher expression ( P < 0.05) of Interferon-gamma, IL-12, IL-23 and GM-CSF were found in Inc- stimulated CD4 enriched cervical cells of CT-positive fertile women and contrastingly high IL-1 Beta, IL-4, IL-5, IL-6 and IL-10 levels were found in CT-positive infertile women. Paper-13972544.
T cell-derived cytokines, such as interleukin-5 ( IL-5) and granulocyte-macrophage colony-stimulating factor ( GM-CSF) activate eosinophils, whereas other cytokines, such as tumor necrosis factor (TNF)-alpha and IL-13, determine eosinophil recruitment. Paper-905627.
METHODS: The authors genotyped seven polymorphisms of the IL13, IL4RA, IL5 and ADRB2 genes in 146 patients allergic to olive pollen with seasonal rhinitis/asthma and 50 controls using the polymerase chain reaction-restriction fragment length polymorphism and real-time polymerase chain reaction techniques. Paper-13638207.
The incubation of asthmatic epithelial cells and dendritic cells with autologous resting CD4-positive T cells and purified extracts of D pteronyssinus induced T cell activation and release of high levels of interleukin-4 ( IL-4) and interleukin-5 ( IL-5). Paper-7813129.
We studied the in vitro effects of granulocyte colony-stimulating factor ( G-CSF), granulocyte-macrophage colony-stimulating factor ( GM-CSF), and interleukin 5 ( IL-5) on nuclear segmentation of neutrophils and eosinophils from three patients with congenital or acquired Pelger-Huët anomaly. Paper-6927430.
In this study, TFalpha1 and TFalpha8 cells with stable overexpression of IL-5 receptor alpha (IL-5Ralpha) subunit in TF-1 cells, a human hematopoietic progenitor cell line which expressed low levels of IL-5Ralpha, were used to explored how IL-5 up-regulate c-Myc and the role of c-Myc in IL-5 signaling. Paper-13682607.
RESULTS: Concentrations of tumor necrosis factor-alpha ( TNF-alpha), interleukin-3 ( IL-3), interleukin-4 ( IL-4), interleukin-5 ( IL-5), and granulocyte/macrophage-colony stimulating factor ( GM-CSF) in the serum were 21 pg/mL, <15 pg/mL, <15 pg/mL, 8 pg/mL, and <5 pg/mL pg/mL, respectively. Paper-8423615.
These results demonstrate that both IL-3 and IL-5, alone and in combination have direct-acting effects on CFU-Eos, with the greatest specificity for stimulation of pure Eos colonies and clusters residing in IL-5, and that IL-3, IL-5, and IL-6, alone and in combination, may play a role in the survival of CFU-Eos. Paper-6630409.
Cells from mf-positive onchocerciasis patients produced significantly less interferon-gamma ( IFN-gamma) ( P < 0.01) and interleukin-5 ( IL-5) ( P < 0.05) in response to OvAg than those taken from endemic controls or post-patent individuals in whom IFN-gamma and IL-5 production was similarly high. Paper-1032624.
Isoelectric focusing demonstrated that T cell growth factor ( TCGF), T cell replacing factor ( TRF), and granulocyte-macrophage colony-stimulating factor ( GM-CSF) derived from concanavalin A-stimulated T cell hybridomas and spleen cells are heterogeneous with respect to charge. Paper-4061216.
CONCLUSION: A significant correlation between BAL CCL5, CCL11, and IL-5 levels and eosinophils in patients with pulmonary fibrosis due to SM gas inhalation has been demonstrated, suggesting that these C-C chemokines and IL-5 contribute to the recruitment of eosinophils cells in the lung in these victims. Paper-12604028.
OBJECTIVES: Th-2 type cytokine production ( Interleukin-4 [ IL-4] and interleukin-5 [ IL5]) has been demonstrated to play a significant role in the pathophysiology of allergic rhinitis ( AR), and the treatment of AR with topical corticosteroids has been shown to reduce the expression of Th-2 type cytokines in vivo. Paper-1817702.
OBJECTIVES: Th-2 type cytokine production ( interleukin-4 [ IL-4] and interleukin-5 [ IL-5]) has been demonstrated to play a significant role in the pathophysiology of allergic rhinitis ( AR), and the treatment of AR with topical corticosteroids has been shown to reduce the expression of Th-2 type cytokines in vivo. Paper-1595503.
OBJECTIVES: Our aim was to evaluate the changes induced by topical steroid treatment to the esophageal epithelial inflammatory eosinophilic and T-cell infiltrate and to IL-5, eotaxin-1/ CCL11, and eotaxin-3/ CCL26 esophageal gene expression levels in patients with eosinophilic esophagitis (EE). Paper-13028633.
Recombinant TAT-Deltap85 inhibited interleukin (IL)-5-stimulated phosphorylation of protein kinase B, a downstream target of PI3K. beta(2)-Integrin-dependent adhesion caused by IL-5 to the plated intracellular adhesion molecule-1 surrogate, bovine serum albumin, was inhibited by TAT-Deltap85 in a concentration-dependent manner. Paper-10774384.
RESULTS: Ragweed stimulation significantly increased the production of the Th2-associated cytokines IL-5, IL-9 and IL-13, the chemokines CCL17 and CCL22 and the regulatory cytokine IL-10 in allergic patients, whereas transforming growth factor-beta ( TGF-beta) production was increased only in normal individuals. Paper-13249880.
IL-1 alpha and IL-6 had little or no effect, alone or in combination with IL-3 and IL-5; however, IL-3, IL-5, and IL-6 each enhanced the number of IL-5-responsive CFU-Eos found after suspension culture compared to control medium, with the individual effects being additive when the molecules were combined. Paper-6630409.
The spontaneous adhesion to fibronectin was higher than to laminin and collagen type I. Both spontaneous adhesion to fibronectin and interleukin-3 ( IL-3), interleukin-5 ( IL-5), granulocyte/macrophage colony stimulating factor ( GM-CSF) induced adhesion to BSA increased with time between 5 and 45 min. Paper-9446729.
The functional receptors for many of these cytokines (e.g., interleukin (IL)-2R and IL-6R) involve two distinct subunits; strikingly, the same beta subunit can interact with distinct alpha subunits to constitute the receptor for different cytokines (e.g., those for IL-3, IL-5, and granulocyte monocyte colony-stimulating factor). Paper-7511311.
In order to explore the role of activator protein-1 ( AP-1) in the transcription of interleukin-5 ( IL-5) gene regulated by protein kinase C (PKC) signal in peripheral blood T lymphocytes from asthmatic patient, T lymphocytes were isolated and purified from peripheral blood of each asthmatic patient. Paper-11533439.
The differentiation of normal human peripheral blood B lymphocytes into plasma cells in vitro, studied in mononuclear cells stimulated with PWM or in purified B cells stimulated with a T cell-replacing factor ( TRF), can be inhibited by both deoxyguanosine (dGuo) and guanosine. Paper-4566100.
Mucosal biopsy specimens were immunostained for IL-1 beta, IL-5, IL-6, IL-8, and TNF-a. In chronic rhinosinusitis subjects, mucosal levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were significantly elevated when compared with control subjects, and levels of IL-5 demonstrated a strong trend toward elevation. Paper-8643252.
We further show that GSK-3 is activated after IL-5 withdrawal, and inhibition of its activity rescues eosinophils from apoptosis. beta-catenin, a direct GSK-3 substrate, is present in the nucleus of IL-5-stimulated eosinophils, but it is translocated to the plasma membrane in the absence of cytokine in a GSK-3-dependent manner. Paper-12131587.
The proximity of the SHC-binding site ((577)Tyr) to the 14-3-3-binding site ((582)HSRSLP(587)) and their conservation between mouse, rat, and human beta(c) but not in other cytokine receptors suggest that they form a distinct motif that may subserve specialized functions associated with the GM-CSF, IL-3, and IL-5 receptors. Paper-2004649.
These results suggest that eosinophilia in the pleural fluid induced by IL-2 injection into the pleural cavity of patients with malignant pleurisy is due to the Eo-CSF activities of various components, including IL-5, IL-3, and GM-CSF, and chemotactic factors for eosinophils induced locally in the pleural cavity by IL-2. Paper-6724069.
Paraffin-embedded specimens from 50 patients diagnosed with peripheral T-cell lymphomas, either unspecified (PTCL-U, n=30) or angioimmunoblastic (AITL, n=20) were morphologically assessed for intra-tumoral eosinophilia and analyzed by immunohistochemistry using specific antibodies directed against TARC, IL-5, RANTES, and eotaxin. Paper-14433984.
We performed reverse transcriptase-polymerase chain reaction and Southern blot to examine gene expression of the cytokines interleukin (IL)-1 beta, IL-6, IL-8, transforming growth factor (TGF)-beta, IL-4, IL-5, and interferon (IFN)-gamma and compared the results with the gene expressions of these cytokines in normal nasal mucosa. Paper-1558882.
Eosinophils are thought to be the major pro-inflammatory effector cell in asthma and their persistence in the airways is probably enhanced by the presence of several asthma-relevant cytokines that prolong eosinophil survival by inhibition of apoptosis (interleukin (IL)-3, IL-5, granulocyte-macrophage colony-stimulating factor, IL-9, IL-13, IL-15). Paper-9805894.
A significant interaction with BMI was only observed for IFNGR2 (rs9808753 P(forinteraction) = .034) and IL7R (rs1494555 P(forinteraction) = .016) for NHL overall; IL7R (rs1494555 P(forinteraction) = .016) and TNF (1799724 P(forinteraction) = .031) for B-cell lymphoma; and IL5 (rs2069812 P(forinteraction) = .034) for T-cell lymphoma. Paper-15619874.
Since the recruitment of inflammatory cells to tissues requires the participation of adhesion molecules, we have developed a rapid and sensitive assay to examine the effect of IL-5 and other activation stimuli on eosinophil adhesion to recombinant intercellular adhesion molecule-1 ( ICAM-1), and vascular cell adhesion molecule-1 ( VCAM-1). Paper-998769.
BGEF-2 itself did not show IL-2 activity nor IL-1 activity, and BGEF-2 activity was not detected in the following cytokines: Interferon-alpha (IFN-alpha), interferon-gamma ( IFN-gamma), tumor necrosis factor ( TNF), interleukin 4 ( IL-4), interleukin 5 ( IL-5) and interleukin 6 ( IL-6). Paper-6416472.
Human recombinant IL-5, granulocyte-macrophage colony stimulating factor ( GM-CSF), interleukin 3 ( IL-3), tumour necrosis factor alpha ( TNF-alpha), RANTES, MCP-3, C5a, PAF, fMLP, PMA and ConA all induced adhesion of purified eosinophils obtained from normal donors to ICAM-1 and VCAM-1 in a dose and time dependent manner. Paper-998769.
Point mutation and reporter ChIP ( chromatin immunoprecipitation) studies determined that the four transcription factors binding on the IL-5 promoter, i.e. C/EBPbeta ( CAAT/enhancer-binding protein beta), GATA3 ( GATA binding protein 3), NFAT (nuclear factor of activated T cells) and YY1 (Yin and Yang 1), were essential for the recruitment of HDAC4. Paper-12324719.
BACKGROUND: We investigated the expressions and ratios of type 1 T helper cell (Th1) cytokines interferon-gamma ( IFN-gamma) and interleukin-2 ( IL-2), as well as type 2 T helper cell (Th2) cytokines interleukin-4 ( IL-4), interleukin-5 ( IL-5), interleukin-13 ( IL-13) and interleukin-10 ( IL-10) in pelvic inflammatory disease (PID) patients. Paper-14473693.
NFAT (nuclear factor of activated T cells) is a transcription factor that plays a role in the regulation of various cytokines, including those involved in the regulation of hemopoetic cells such as granulocyte-macrophage colony stimulating factor ( GM-CSF), interleukin-4 ( IL4), interleukin-3 ( IL3), interleukin-13 ( IL13) and interleukin-5 ( IL5). Paper-2092885.
These data suggest IL-5-specific signaling, not shared by IL-3 and GM-CSF, leading to a switch toward up-regulation of functional IL-5Ralpha and, furthermore, that IL-3 and GM-CSF-driven eosinophil development is dependent on IL-5, providing an explanation for the selective requirement of IL-5 for expansion of the eosinophil lineage. Paper-2144149.
While recombinant human interleukin-2 ( IL-2), interleukin-3 ( IL-3), interleukin-4 ( IL-4), interleukin-5 ( IL-5), interleukin-6 ( IL-6), and rat or human recombinant interferon-gamma ( IFN-gamma) have no proliferative effect on astrocytes, a human T cell-derived B cell growth factor ( BCGF) does. Paper-6172094.
These synonyms are used for gene IL5 (interleukin 5 (colony-stimulating factor, eosinophil)): TRF, T-cell replacing factor, Interleukin-5, IL-5, Eosinophil differentiation factor, EDF, B-cell differentiation factor I.
These accession numbers are used for gene IL5: X04688 (NCBI_GENBANK__AC), Q13840 (UNIPROT__AC), C9JQP9 (UNIPROT__AC), BC066280 (NCBI_GENBANK__AC).
IL5 is a homologue of IL5 (interleukin 5 (colony-stimulating factor, eosinophil)) from Pan troglodytes.
IL5 is a homologue of IL5 (interleukin 5 (colony-stimulating factor, eosinophil)) from Canis lupus familiaris.
IL5 is a homologue of IL5 (interleukin 5 (colony-stimulating factor, eosinophil)) from Bos taurus.
IL5 is a homologue of Il5 (interleukin 5) from Mus musculus.
IL5 is a homologue of Il5 (interleukin 5) from Rattus norvegicus.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.