Human regulatory T cells in autoimmune diseases

被引:71
作者
Cvetanovich, Gregory L. [1 ]
Hafler, David A. [1 ,2 ,3 ]
机构
[1] Harvard Univ, Sch Med, Boston, MA 02215 USA
[2] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06520 USA
[3] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA
基金
美国国家卫生研究院;
关键词
REMITTING MULTIPLE-SCLEROSIS; FOXP3; EXPRESSION; SUPPRESSIVE FUNCTION; DNA METHYLATION; IN-VITRO; LUPUS-ERYTHEMATOSUS; PERIPHERAL-BLOOD; GRANZYME-B; EX-VIVO; NAIVE;
D O I
10.1016/j.coi.2010.08.012
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Human regulatory T cells (Tregs) play a critical role in preventing autoimmunity, and their failure contributes to autoimmune diseases. In recent years, our understanding of human Tregs has been greatly enhanced by improvements in the definition and isolation of pure human Tregs, as well as by the discovery of phenotypically and functionally distinct human Treg subsets. This progress has also yielded a better understanding of the mechanisms of human Treg suppression and the role of human Tregs in autoimmune diseases. An unexpected discovery is that human Tregs have considerable plasticity that allows them to produce the pro-inflammatory cytokine IL-17 under certain conditions. These recent advances highlight the importance of studying the roles of both mouse and human Tregs in autoimmunity.
引用
收藏
页码:753 / 760
页数:8
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