Differential cell-intrinsic regulations of germinal center B and T cells by miR-146a and miR-146b

Sunglim Cho, Hyang-Mi Lee, I-Shing Yu, Youn Soo Choi, Hsi-Yuan Huang, Somaye Sadat Hashemifar, Ling-Li Lin, Mei-Chi Chen, Nikita D. Afanasiev, Aly Azeem Khan, Shu-Wha Lin, Alexander Y. Rudensky, Shane Crotty and Li-Fan Lu ()
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Sunglim Cho: University of California
Hyang-Mi Lee: University of California
I-Shing Yu: National Taiwan University
Youn Soo Choi: La Jolla Institute for Allergy and Immunology
Hsi-Yuan Huang: China Medical University Hospital, China Medical University
Somaye Sadat Hashemifar: Toyota Technological Institute
Ling-Li Lin: University of California
Mei-Chi Chen: University of California
Nikita D. Afanasiev: University of California
Aly Azeem Khan: Toyota Technological Institute
Shu-Wha Lin: National Taiwan University
Alexander Y. Rudensky: Memorial Sloan-Kettering Cancer Center
Shane Crotty: La Jolla Institute for Allergy and Immunology
Li-Fan Lu: University of California

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-05196-3

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