Negative Regulation of Cytokine Signaling in Immunity
Negative Regulation of Cytokine Signaling in Immunity
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DOI：
10.1101/cshperspect.a028571
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发表时间：
2018-07-01
影响因子：
7.2
通讯作者：
Nakatsukasa, Hiroko
中科院分区：
文献类型：
--
作者：
Yoshimura, Akihiko;Ito, Minako;Nakatsukasa, Hiroko
细胞因子是免疫的关键调节剂。大多数细胞因子使用 Janus 激酶和信号转导子和转录激活子 (JAK-STAT) 途径来促进基因转录调节，但它们的信号必须通过多种机制减弱。其中包括细胞因子信号传导抑制蛋白 (SOCS) 家族蛋白，它们代表了 JAK-STAT 通路的主要负调节机制。含细胞因子诱导的 Src 同源 2 (SH2) 蛋白 (CIS)、SOCS1 和 SOCS3 蛋白调节细胞因子信号，控制 CD4(+) thorn T 细胞的极化和 CD8(+) thorn T 细胞的成熟。 SOCS 蛋白还调节先天免疫细胞并参与肿瘤发生。本文综述了 CIS、SOCS1 和 SOCS3 在 T 细胞和肿瘤免疫中的最新进展。
Cytokines are key modulators of immunity. Most cytokines use the Janus kinase and signal transducers and activators of transcription (JAK-STAT) pathway to promote gene transcriptional regulation, but their signals must be attenuated by multiple mechanisms. These include the suppressors of cytokine signaling (SOCS) family of proteins, which represent a main negative regulation mechanism for the JAK-STAT pathway. Cytokine-inducible Src homology 2 (SH2)-containing protein (CIS), SOCS1, and SOCS3 proteins regulate cytokine signals that control the polarization of CD4(+) thorn T cells and the maturation of CD8(+) thorn T cells. SOCS proteins also regulate innate immune cells and are involved in tumorigenesis. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in T cells and tumor immunity.