通过 ITK 调节辅助性 T 细胞分化。
Tuning T helper cell differentiation by ITK.
机构信息
Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, U.S.A.
Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, U.S.A.
出版信息
Biochem Soc Trans. 2020 Feb 28;48(1):179-185. doi: 10.1042/BST20190486.
Abstract
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 TH17, 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.
摘要
CD4+效应 T 细胞实现 T 细胞免疫应答，产生细胞因子来协调免疫应答的性质和类型。非受体酪氨酸激酶白细胞介素 2 诱导的 T 细胞激酶 (ITK) 是 T 细胞受体信号转导的介质，在调节这些效应细胞的发育中起着关键作用。在这篇综述中，我们讨论了 ITK 下游信号（包括 Ras/MAPK 途径）在差异控制 TH17、Foxp3+T 调节（Treg）细胞和 1 型调节性 T（Tr1）细胞分化中的作用，支持 ITK 信号控制效应 T 细胞分化过程中的决策点的模型。
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本文引用的文献
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2
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