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miR-132 suppresses transcription of ribosomal proteins to promote protective Th1 immunity. | LitMetric

miR-132 suppresses transcription of ribosomal proteins to promote protective Th1 immunity.

EMBO Rep

Centre for Immunology and Infection and York Biomedical Research Institute, Hull York Medical School and Department of Biology, University of York, York, UK

Published: April 2019

AI Article Synopsis

Article Abstract

Determining the mechanisms that distinguish protective immunity from pathological chronic inflammation remains a fundamental challenge. miR-132 has been shown to play largely immunoregulatory roles in immunity; however, its role in CD4 T cell function is poorly understood. Here, we show that CD4 T cells express high levels of miR-132 and that T cell activation leads to miR-132 up-regulation. The transcriptomic hallmark of splenic CD4 T cells lacking the miR-132/212 cluster during chronic infection is an increase in mRNA levels of ribosomal protein (RP) genes. BTAF1, a co-factor of B-TFIID and novel miR-132/212-3p target, and p300 contribute towards miR-132/212-mediated regulation of RP transcription. Following infection with CD4 T cells display enhanced expression of IL-10 and decreased IFNγ. This is associated with reduced hepatosplenomegaly and enhanced pathogen load. The enhanced IL-10 expression in Th1 cells is recapitulated following treatment with phenylephrine, a drug reported to promote ribosome synthesis. Our results uncover that miR-132/212-mediated regulation of RP expression is critical for optimal CD4 T cell activation and protective immunity against pathogens.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446204PMC
http://dx.doi.org/10.15252/embr.201846620DOI Listing

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