T细胞受体
生物
CD3型
细胞生物学
跨膜蛋白
胆固醇
生物化学
受体
T细胞
抗原
免疫系统
免疫学
CD8型
作者
Yan Chen,Yuwei Zhu,Xiang Li,Wenbo Gao,Ziqi Zhen,De Dong,Buliao Huang,Zhuo Ma,Anqi Zhang,Xiaocui Song,Yan Ma,Changyou Guo,Fan Zhang,Zhiwei Huang
出处
期刊:Molecular Cell
[Elsevier]
日期:2022-03-09
卷期号:82 (7): 1278-1287.e5
被引量:55
标识
DOI:10.1016/j.molcel.2022.02.017
摘要
Cholesterol molecules specifically bind to the resting αβTCR to inhibit cytoplasmic CD3ζ ITAM phosphorylation through sequestering the TCR-CD3 complex in an inactive conformation. The mechanisms of cholesterol-mediated inhibition of TCR-CD3 and its activation remain unclear. Here, we present cryoelectron microscopy structures of cholesterol- and cholesterol sulfate (CS)-inhibited TCR-CD3 complexes and an auto-active TCR-CD3 variant. The structures reveal that cholesterol molecules act like a latch to lock CD3ζ into an inactive conformation in the membrane. Mutations impairing binding of cholesterol molecules to the tunnel result in the movement of the proximal C terminus of the CD3ζ transmembrane helix, thereby activating the TCR-CD3 complex in human cells. Together, our data reveal the structural basis of TCR inhibition by cholesterol, illustrate how the cholesterol-binding tunnel is allosterically coupled to TCR triggering, and lay a foundation for the development of immunotherapies through directly targeting the TCR-CD3 complex.
科研通智能强力驱动
Strongly Powered by AbleSci AI