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PMID |
Sentence |
| 1 |
12508169
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Cytokines produced by type 2 Th (Th2) lymphocytes, such as interleukin (IL)-4, IL-5, and IL-13), predominate in membranous GN and in minimal change disease.
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| 2 |
12508169
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Interactions between IP-10/CXCL10, Mig/CXCL9 and I-TAC/CXCL11 and their shared receptor, CXCR3, seem to be responsible not only for Th1 cell infiltration in acute allograft rejection and in proliferative GN, but also for mesangial cell proliferation typical of the latter condition.
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| 3 |
12508169
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Moreover, in the kidneys of subjects suffering from chronic allograft nephropathy, IP-10/CXCL10, Mig/CXCL9 and I-TAC/CXCL11 have been found to be produced by and to act on the proxymal tubular epithelial cells, endothelial cells and smooth muscle vessel cells, suggesting their possible role in both the genesis of tubular atrophy and allograft artheriosclerosis.
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| 4 |
17611223
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The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
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| 5 |
17611223
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The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development.
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| 6 |
17611223
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Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage.
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| 7 |
17611223
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Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy.
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| 8 |
21744329
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Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis.
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| 9 |
21744329
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The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human.
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| 10 |
21744329
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Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13.
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| 11 |
23755752
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Histone modifications of Notch1 promoter affect lung CD4+ T cell differentiation in asthmatic rats.
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| 12 |
23755752
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The present study aimed to explore the histone modifications of Notch1 promoter in normal and asthmatic lung CD4+ T cells.
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| 13 |
23755752
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Chromatin immunoprecipitation analysis showed that the acetylation levels of total H3, H4, site-specific H3K9, H3K14, H3K27, H3K18, H4K16, and the trimethylation levels of H3K4, H3K79 of Notch1 gene promoter were increased significantly in asthmatic lung CD4+ T cells compared to the control group, which correlated with increased P300, PCAF activity and decreased HDAC1, HDAC2 activity.
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| 14 |
23755752
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After intervention of garcinol, a potent inhibitor of histone acetyltransferases, in asthmatic lung CD4+ T cells, HAT activity decreased significantly and the increased Notch1 and hes-1 expression was reversed.
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| 15 |
23755752
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Results showed that the levels of IL-4, IL-5 and IL-13 were significantly reduced and a small reverse trend was found in the level of IFN-g after GAR treatment.
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| 16 |
23761633
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STAT4 and T-bet are required for the plasticity of IFN-γ expression across Th2 ontogeny and influence changes in Ifng promoter DNA methylation.
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| 17 |
23761633
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CD4(+) T cells developing toward a Th2 fate express IL-4, IL-5, and IL-13 while inhibiting production of cytokines associated with other Th types, such as the Th1 cytokine IFN- γ.
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| 18 |
23761633
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We now show that this flexibility ("plasticity") of cytokine expression is preceded by a loss of the repressive DNA methylation of the Ifng promoter acquired during Th2 polarization yet requires STAT4 along with T-box expressed in T cells.
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| 19 |
23761633
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Surprisingly, loss of either STAT4 or T-box expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells.
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| 20 |
23831616
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Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11.
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| 21 |
23831616
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However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected.
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| 22 |
24167278
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Gata3/Ruvbl2 complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.
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| 23 |
24167278
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GATA-binding protein 3 (Gata3) controls the differentiation of naive CD4 T cells into T helper 2 (Th2) cells by induction of chromatin remodeling of the Th2 cytokine gene loci, direct transactivation of Il5 and Il13 genes, and inhibition of Ifng.
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| 24 |
24167278
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We herein found that Gata3 associates with RuvB-like protein 2 (Ruvbl2) and represses the expression of a CDK inhibitor, cyclin-dependent kinase inhibitor 2c (Cdkn2c) to facilitate the proliferation of Th2 cells.
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| 25 |
24167278
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Gata3 directly bound to the Cdkn2c locus in an Ruvbl2-dependent manner.
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| 26 |
24167278
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We therefore have identified a functional Gata3/Ruvbl2 complex that regulates the proliferation of differentiating Th2 cells through the repression of a CDK inhibitor, Cdkn2c.
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