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10.1038/ncomms7436 http://scihub22266oqcxt.onion/10.1038/ncomms7436 C4366510!4366510 !25743066     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25743066 &cmd=llinks): Failed to open stream: HTTP request failed! 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MicroRNA-146a regulates ICOS-ICOSL signalling to limit accumulation of T follicular helper cells and germinal centres |pdf=|usr=}}{{25743066 }} gab.com Text MicroRNA-146a regulates ICOS-ICOSL signalling to limit accumulation of T follicular helper cells and germinal centres JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25743066 #FOAvip 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 addition, miR-146a deficiency leads to increased ICOSL expression on GC B cells and antigen-presenting cells. 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. Twit Text FOAVip MicroRNA-146a regulates ICOS-ICOSL signalling to limit accumulation of T follicular helper cells and germinal centres ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25743066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25743066 #FOAvip English Wikipedia <ref>{{Cite pmid|25743066 }}</ref> MicroRNA-146a regulates ICOS-ICOSL signalling to limit accumulation of T follicular helper cells and germinal centres #MMPMID25743066 Pratama A ; Srivastava M ; Williams NJ ; Papa I ; Lee SK ; Dinh XT ; Hutloff A ; Jordan MA ; Zhao JL ; Casellas R ; Athanasopoulos V ; Vinuesa CG Nat Commun 2015[Mar]; 6 (ä): 6436 PMID25743066 show ga 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 addition, miR-146a deficiency leads to increased ICOSL expression on GC B cells and antigen-presenting cells. 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. |Adoptive Transfer [MESH] |Animals [MESH] |Cell Differentiation/*immunology [MESH] |DNA Primers/genetics [MESH] |Flow Cytometry [MESH] |Germinal Center/*immunology [MESH] |Humans [MESH] |Inducible T-Cell Co-Stimulator Ligand/*metabolism [MESH] |Inducible T-Cell Co-Stimulator Protein/*metabolism [MESH] |Luciferases [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |MicroRNAs/*metabolism [MESH] |Palatine Tonsil/cytology [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Signal Transduction/*immunology [MESH] |Statistics, Nonparametric [MESH]MicroRNA-146a regulates ICOS-ICOSL signalling to limit accumulation of(epmc).pdf DeepDyve Pubget Overpricing