CD4 T-cell differentiation and inflammatory bowel disease

被引:252
|
作者
Zenewicz, Lauren A. [1 ]
Antov, Andrey [1 ]
Flavell, Richard A. [1 ,2 ]
机构
[1] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA
关键词
ACTIVE CROHNS-DISEASE; GROWTH-FACTOR-BETA; ROR-GAMMA-T; ARYL-HYDROCARBON RECEPTOR; TYPE-1 CYTOKINE RESPONSES; TGF-BETA; TH17; CELLS; INTESTINAL INFLAMMATION; EXPERIMENTAL COLITIS; ULCERATIVE-COLITIS;
D O I
10.1016/j.molmed.2009.03.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Differentiation of naive T cells leads to the generation of T-cell subsets, each possessing distinct cytokine expression profiles for serving different immune functions. Through the activation of separate signaling pathways, this process results in both differentiated helper T (Th) cells, termed Th1, Th2 and Th17, and induced regulatory T cells, which suppress Th cells. These different cells are important for combating infectious diseases and cancers; however, when aberrant, they can be responsible for chronic inflammatory diseases. One such disease is inflammatory bowel disease (IBD), in which each T-cell subset can have a role in disease. New studies highlight the importance of the recently identified Th17 subset in IBD. Therapeutics targeting these aberrant Th responses are already under development and hold promise for treating IBD and other chronic inflammatory diseases.
引用
收藏
页码:199 / 207
页数:9
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