Repression of miR-31 by BCL6 stabilizes the helper function of human follicular helper T cells

Anna Ripamonti(Istituto Nazionale Genetica Molecolare), Elena Provasi(Istituto Nazionale Genetica Molecolare), M. Rosario Lorenzo(Istituto Nazionale Genetica Molecolare), Marco De Simone(Istituto Nazionale Genetica Molecolare), Valeria Ranzani(Istituto Nazionale Genetica Molecolare), Silvia Vangelisti(Istituto Nazionale Genetica Molecolare), Serena Maria Curti(Istituto Nazionale Genetica Molecolare), Raoul J.P. Bonnal(Istituto Nazionale Genetica Molecolare), Lorenzo Pignataro(University of Milan), Sara Torretta(University of Milan), Jens Geginat(Istituto Nazionale Genetica Molecolare), Grazisa Rossetti(Istituto Nazionale Genetica Molecolare), Massimiliano Pagani(University of Milan), Sergio Abrignani(University of Milan)
Proceedings of the National Academy of Sciences
November 13, 2017
Cited by 36Open Access
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Abstract

Significance Antibody production by B lymphocytes generally requires help by T follicular helper (T FH ) cells, a specific subset of CD4 + T lymphocytes. The function of T FH cells depends on BCL6, a transcriptional repressor whose target genes that account for the helper activity are unknown. By the combined analysis of microRNA (miRNA) and gene expression profiling in human T FH cells, we found that miR-31, a miRNA that inhibits gene transcripts relevant for T FH cells biology, is down-regulated in T FH . BCL6 contributes to “helperness” by shutting down miR-31 gene expression, thus stabilizing the follicular helper T cell program. Thus miR-31 is a therapeutic target to modulate human T cell-dependent antibody responses in immunomediated disorders.


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