生物
自身免疫
T细胞受体
免疫系统
免疫学
T细胞
周边公差
自身免疫性疾病
信号转导
受体
免疫耐受
共刺激
获得性免疫系统
癌症研究
细胞毒性T细胞
中心公差
免疫
细胞生物学
细胞信号
否定选择
表型
调节性T细胞
克隆缺失
免疫受体
免疫疗法
癌症
CTLA-4号机组
细胞
作者
Atsushi Tanaka,Shimon Sakaguchi
标识
DOI:10.1146/annurev-immunol-082724-025403
摘要
The intensity of T cell receptor (TCR) signaling controls thymic positive and negative selection of conventional T cells (Tconv cells) and regulatory T cells (Treg cells), as well as their peripheral activation. Accordingly, the effects of graded TCR signal reduction manifest as a disease spectrum encompassing T cell immune deficiency, latent autoimmunity, and overt autoimmune disease. TCR signal attenuation to a certain range-for example, through hypomorphic mutation of the ZAP-70 (ζ chain-associated protein-70) molecule or reduced expression of its normal form-shifts the TCR repertoire of Tconv and Treg cells toward higher self-reactivity and hampers Treg cell generation. These alterations together lead to spontaneous development of various T cell-mediated autoimmune and inflammatory diseases. Additional host genetic and environmental factors exert secondary effects on disease phenotype and manifestation. In addition, pharmacological attenuation of TCR signaling to a certain range in peripheral T cells can selectively reduce mature Treg cells and evoke effective antitumor immune responses. Collectively, TCR-proximal signaling is a key target for controlling autoimmunity and cancer immunity.
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