Mechanisms Underlying Lineage Commitment and Plasticity of Helper CD4+ T Cells

被引:1006
作者
O'Shea, John J. [1 ]
Paul, William E. [1 ]
机构
[1] NIAID, Mol Immunol & Inflammat Branch, NIAMSD, Immunol Lab,NIH, Bethesda, MD 20892 USA
关键词
ROR-GAMMA-T; TH17; CELLS; FATE DETERMINATION; INTERLEUKIN; 22; TGF-BETA; DIFFERENTIATION; INFLAMMATION; LYMPHOCYTES; GENERATION; POPULATION;
D O I
10.1126/science.1178334
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
CD4(+) T cells are critical for host defense but are also major drivers of immune-mediated disease. These T cells specialize to become distinct subsets and produce restricted patterns of cytokines, which are tailored to combat various microbial pathogens. Although classically viewed as distinct lineages, recent work calls into question whether helper CD4(+) T cell subsets are more appropriately viewed as terminally differentiated cells or works in progress. Herein, we review recent advances that pertain to this topic and the mechanisms that contribute to helper CD4(+) T cell commitment and plasticity. The therapeutic implications of these new findings are also considered.
引用
收藏
页码:1098 / 1102
页数:5
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