MicroRNA-146a regulates ICOS–ICOSL signalling to limit accumulation of T follicular helper cells and germinal centres

Journal Publication ResearchOnline@JCU
Pratama, Alvin;Srivastava, Monika;Williams, Naomi J.;Papa, Ilenia;Lee, Sau K.;Dinh, Xuyen T.;Hutloff, Andreas;Jordan, Margaret A.;Zhao, Jimmy L.;Casellas, Rafael;Athanasopoulos, Vicki;Vinuesa, Carola G.
Abstract

Tight control of T follicular helper (Tfh) cells is required for optimal maturation of the germinal centre (GC) response. The molecular mechanisms controlling Tfh-cell differentiation remain incompletely understood. Here we show that microRNA-146a (miR-146a) is highly expressed in Tfh cells and peak miR-146a expression marks the decline of the Tfh response after immunization. Loss of miR-146a causes cell-intrinsic accumulation of Tfh and GC B cells. MiR-146a represses several Tfh-cell-expressed messenger RNAs, and of these, ICOS is the most strongly cell autonomously upregulated target in miR-146a-deficient T cells. In ddition,miR-146a deficiency leads to increased ICOSL expression on GC B cells and antigenpresentingcells. Partial blockade of ICOS signalling, either by injections of low dose of ICOSL blocking antibody or by halving the gene dose of Icos in miR-146a-deficient T cells, prevents the Tfh and GC B-cell accumulation. Collectively, miR-146a emerges as a post-transcriptional brake to limit Tfh cells and GC responses.

Journal

Nature Communications

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6

ISBN/ISSN

2041-1723

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Pages Count

14

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Nature Publishing Group

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DOI

10.1038/ncomms7436