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10.4049/jimmunol.1601882

http://scihub22266oqcxt.onion/10.4049/jimmunol.1601882
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C5502319!5502319!28607112
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suck abstract from ncbi


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pmid28607112      J+Immunol 2017 ; 199 (2): 391-6
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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 #MMPMID28607112
  • Dedobbeleer O; Stockis J; van der Woning B; Coulie PG; Lucas S
  • J Immunol 2017[Jul]; 199 (2): 391-6 PMID28607112show 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.
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