生发中心
自身免疫
体液免疫
CD40
生物
B细胞
免疫学
细胞生物学
抗体
遗传学
细胞毒性T细胞
体外
作者
Sunglim Cho,Hyang‐Mi Lee,I‐Shing Yu,Youn Soo Choi,Hsi‐Yuan Huang,Somaye Hashemifar,Ling-Li Lin,Mei‐Chi Chen,Nikita D. Afanasiev,Aly A. Khan,Shu‐Wha Lin,Alexander Y. Rudensky,Shane Crotty,Li‐Fan Lu
标识
DOI:10.1038/s41467-018-05196-3
摘要
Reciprocal interactions between B and follicular T helper (Tfh) cells orchestrate the germinal center (GC) reaction, a hallmark of humoral immunity. Abnormal GC responses could lead to the production of pathogenic autoantibodies and the development of autoimmunity. Here we show that miR-146a controls GC responses by targeting multiple CD40 signaling pathway components in B cells; by contrast, loss of miR-146a in T cells does not alter humoral responses. However, specific deletion of both miR-146a and its paralog, miR-146b, in T cells increases Tfh cell numbers and enhanced GC reactions. Thus, our data reveal differential cell-intrinsic regulations of GC B and Tfh cells by miR-146a and miR-146b. Together, members of the miR-146 family serve as crucial molecular brakes to coordinately control GC reactions to generate protective humoral responses without eliciting unwanted autoimmunity.
科研通智能强力驱动
Strongly Powered by AbleSci AI