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10.4049/jimmunol.1601882 http://scihub22266oqcxt.onion/10.4049/jimmunol.1601882 C5502319!5502319 !28607112     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28607112 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cutting Edge: Active TGF-?1 Released from GARP/TGF-?1 Complexes on the Surface of Stimulated Human B Lymphocytes Increases Class-Switch Recombination and Production of IgA |pdf=|usr=}}{{28607112 }} gab.com Text Cutting Edge: Active TGF- 1 Released from GARP/TGF- 1 Complexes on the Surface of Stimulated Human B Lymphocytes Increases Class-Switch Recombination and Production of IgA JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28607112 #FOAvip Production of active TGF-? is regulated at a posttranslational level and implies release of the mature cytokine dimer from the inactive, latent TGF-? precursor. There are several cell-type specific mechanisms of TGF-? activation. We identified a new mechanism operating on the surface of human regulatory T cells and involving membrane protein GARP, which binds latent TGF-?1. The paracrine activity of regulatory T cell-derived TGF-?1 contributes to immunosuppression and can be inhibited with anti-GARP Abs. Whether other immune cell types use surface GARP to activate latent TGF-?1 was not known. We show in this study that stimulated, human B lymphocytes produce active TGF-?1 from surface GARP/latent TGF-?1 complexes with isotype switching to IgA production. Twit Text FOAVip Cutting Edge: Active TGF- 1 Released from GARP/TGF- 1 Complexes on the Surface of Stimulated Human B Lymphocytes Increases Class-Switch Recombination and Production of IgA ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28607112 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28607112 #FOAvip English Wikipedia <ref>{{Cite pmid|28607112 }}</ref> Cutting Edge: Active TGF-?1 Released from GARP/TGF-?1 Complexes on the Surface of Stimulated Human B Lymphocytes Increases Class-Switch Recombination and Production of IgA #MMPMID28607112 Dedobbeleer O ; Stockis J ; van der Woning B ; Coulie PG ; Lucas S J Immunol 2017[Jul]; 199 (2 ): 391-396 PMID28607112 show ga Production of active TGF-? is regulated at a posttranslational level and implies release of the mature cytokine dimer from the inactive, latent TGF-? precursor. There are several cell-type specific mechanisms of TGF-? activation. We identified a new mechanism operating on the surface of human regulatory T cells and involving membrane protein GARP, which binds latent TGF-?1. The paracrine activity of regulatory T cell-derived TGF-?1 contributes to immunosuppression and can be inhibited with anti-GARP Abs. Whether other immune cell types use surface GARP to activate latent TGF-?1 was not known. We show in this study that stimulated, human B lymphocytes produce active TGF-?1 from surface GARP/latent TGF-?1 complexes with isotype switching to IgA production. |*Immunoglobulin Class Switching [MESH] |B-Lymphocytes/drug effects/*immunology [MESH] |Cytokines/immunology [MESH] |Humans [MESH] |Immunoglobulin A/*biosynthesis/immunology [MESH] |Lymphocyte Activation [MESH] |Membrane Proteins/*metabolism [MESH] |Oligodeoxyribonucleotides/immunology [MESH] |Protein Binding [MESH] |Recombination, Genetic [MESH] |T-Lymphocytes, Regulatory/immunology [MESH]Cutting Edge: Active TGF-?1 Released from GARP/TGF-?1 Complexes on the(epmc).pdf DeepDyve Pubget Overpricing