期刊
JOURNAL OF IMMUNOLOGY
卷 176, 期 6, 页码 3470-3479出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.176.6.3470
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- Medical Research Council [MC_U117565642] Funding Source: Medline
- MRC [MC_U117565642] Funding Source: UKRI
- Medical Research Council [MC_U117565642] Funding Source: researchfish
IL-10 is a major regulator in inflammatory responses. Although various transcription factors were defined to enhance IL-10, the molecular mechanism for the initiation of Il-10 transcription, remains unknown. mRNA profiling of six distinct primary CD4(+) T cell populations showed differential expression of the transcription factor GATA-3 correlated with levels of IL-10 expression. We showed that ectopic expression of GATA-3 in naive primary CD4(+) T cells enhanced expression of IL-10 by these cells and uncovered a possible mechanism for this effect. We found that GATA-3 induced changes of the chromatin structure at the Il-10 locus and that these changes occur even in the absence of IL-4. Furthermore we found that in the presence of GATA-3 the histones at the Il-10 locus become acetylated. Despite being recruited in vivo to two locations on the Il-10 locus, GATA-3 did not transactivate the IL-10 promoter. We therefore suggest a key role of GATA-3 in instructing Il-10 gene expression in primary CD4(+) T cells, possibly by switching and stabilizing the Il-10 locus into a transcriptionally competent status.
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