作者: Charles Sia
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摘要: Controlling the diabetogenic activity of peripheral islet antigen-specific T cells is essential to halt progression autoimmunity that leads development type 1 diabetes mellitus (T1DM). Over past years, evidence has been gathered suggest dysfunction CD4(+)CD25(+) regulatory (Treg) cells, and interleukin-10 (IL10) -secreting (Tr1) are associated with disease onset in diabetic patients. Although Treg develop as a distinct lineage thymus, results from recent studies have shown they can also arise independently pool conventional CD4(+) lymphocytes. These observations led various methods convert into Tr1 vitro or induce expansion cell subsets vivo. This article reviews progress made recruitment vivo involves potential for prevention even reversal T1DM.