Cell type-specific regulation of IL-10 expression in inflammation and disease

被引:178
作者
Hedrich, Christian M. [1 ]
Bream, Jay H. [1 ]
机构
[1] Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA
关键词
IL-10; Inflammation; Human; Immunoregulation; Gene expression; Polymorphism; Transgenic; SNP; TUMOR-NECROSIS-FACTOR; SINGLE NUCLEOTIDE POLYMORPHISMS; INTERLEUKIN-10 PROTECTS MICE; INHIBITS CYTOKINE PRODUCTION; CENTRAL-NERVOUS-SYSTEM; IFN-GAMMA EXPRESSION; NATURAL-KILLER-CELLS; HUMAN NK CELLS; T-HELPER-CELL; GENE-EXPRESSION;
D O I
10.1007/s12026-009-8150-5
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
IL-10 plays an essential part in controlling inflammation and instructing adaptive immune responses. Consequently, dysregulation of IL-10 is linked with susceptibility to numerous infectious and autoimmune diseases in mouse models and in humans. It has become increasingly clear that appropriate temporal/spatial expression of IL-10 may be the key to how IL-10 contributes to the delicate balance between inflammation and immunoregulation. The mechanisms that govern the cell type- and receptor-specific induction of IL-10, however, remain unclear. This is due largely to the wide distribution of cellular sources that express IL-10 under diverse stimulation conditions and in a variety of tissue compartments. Further complicating the issue is the fact that human IL-10 expression patterns appear to be under genetic influence resulting in differential expression and disease susceptibility. In this review, we discuss the cellular sources of IL-10, their link to disease phenotypes and the molecular mechanisms implicated in IL-10 regulation.
引用
收藏
页码:185 / 206
页数:22
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