Tuning T helper cell differentiation by ITK

被引:22
|
作者
Elmore, Jessica P. [1 ]
McGee, Michael C. [2 ]
Nidetz, Natalie F. [2 ]
Anannya, Orchi [1 ]
Huang, Weishan [1 ,2 ]
August, Avery [1 ]
机构
[1] Cornell Univ, Dept Microbiol & Immunol, Ithaca, NY 14853 USA
[2] Louisiana State Univ, Sch Vet Med, Dept Pathobiol Sci, Baton Rouge, LA 70803 USA
基金
美国国家卫生研究院;
关键词
PROTEIN-TYROSINE KINASE; FOXP3; EXPRESSION; SIGNAL-TRANSDUCTION; RECEPTOR; TH17; ACTIVATION; CD4(+); MICE; INDUCTION; REQUIREMENT;
D O I
10.1042/BST20190486
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
CD4(+) effector T cells effectuate T cell immune responses, producing cytokines to orchestrate the nature and type of immune responses. The non-receptor tyrosine kinase IL-2 inducible T cell kinase (ITK), a mediator of T cell Receptor signaling, plays a critical role in tuning the development of these effector cells. In this review we discussed the role that signals downstream of ITK, including the Ras/MAPK pathway, play in differentially controlling the differentiation of T(H)17, Foxp3(+) T regulatory (Treg) cells, and Type 1 regulatory T (Tr1) cells, supporting a model of ITK signals controlling a decision point in the effector T cell differentiation process.
引用
收藏
页码:179 / 185
页数:7
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