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

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2020年 / 48卷 / 01期

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

页码：179 / 185

页数：7

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