期刊
JOURNAL OF IMMUNOLOGY
卷 175, 期 2, 页码 1041-1046出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.2.1041
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资金
- Medical Research Council [MC_U117565642, MC_U117512796] Funding Source: researchfish
- Medical Research Council [MC_U117512796, MC_U117565642] Funding Source: Medline
- NHLBI NIH HHS [HL 59838] Funding Source: Medline
- MRC [MC_U117565642, MC_U117512796] Funding Source: UKRI
The molecular mechanisms that regulate expression of the immunosuppressive cytokine IL-10 remain poorly understood. In this study, by measuring sensitivity to DNase I digestion, we show that production of IL-10 by primary mouse bone marrow-derived macrophages stimulated through pattern recognition receptors was associated with chromatin remodeling of the IL-10 locus. We also demonstrate that the IL-10 locus is remodeled in primary Th2 cells and IL-10-producing regulatory T cells that have been differentiated in vitro. Strikingly, a novel DNase I-hypersensitive site (HSS-4.5) was identified in stimulated macrophages, but not in T cells. We show that hyperacetylated histones were recruited to this site in stimulated macrophages. Furthermore, HSS-4.5 is highly conserved and contains a putative NF-kappa B binding site. In support of a function for this site, NF-kappa B p65/RelA was recruited to HSS-4.5 in vivo and its activation was required for optimal IL-10 gene expression in LPS-stimulated macrophages.
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