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10.1038/s41467-018-05167-8

http://scihub22266oqcxt.onion/10.1038/s41467-018-05167-8
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C6054648!6054648!30030423
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suck abstract from ncbi


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pmid30030423      Nat+Commun 2018 ; 9 (ä): ä
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  • TIGIT+ iTregs elicited by human regulatory macrophages control T cell immunity #MMPMID30030423
  • Riquelme P; Haarer J; Kammler A; Walter L; Tomiuk S; Ahrens N; Wege AK; Goecze I; Zecher D; Banas B; Spang R; Fändrich F; Lutz MB; Sawitzki B; Schlitt HJ; Ochando J; Geissler EK; Hutchinson JA
  • Nat Commun 2018[]; 9 (ä): ä PMID30030423show ga
  • Human regulatory macrophages (Mreg) have shown early clinical promise as a cell-based adjunct immunosuppressive therapy in solid organ transplantation. It is hypothesised that recipient CD4+ T cell responses are actively regulated through direct allorecognition of donor-derived Mregs. Here we show that human Mregs convert allogeneic CD4+ T cells to IL-10-producing, TIGIT+ FoxP3+-induced regulatory T cells that non-specifically suppress bystander T cells and inhibit dendritic cell maturation. Differentiation of Mreg-induced Tregs relies on multiple non-redundant mechanisms that are not exclusive to interaction of Mregs and T cells, including signals mediated by indoleamine 2,3-dioxygenase, TGF-?, retinoic acid, Notch and progestagen-associated endometrial protein. Preoperative administration of donor-derived Mregs to living-donor kidney transplant recipients results in an acute increase in circulating TIGIT+ Tregs. These results suggest a feed-forward mechanism by which Mreg treatment promotes allograft acceptance through rapid induction of direct-pathway Tregs.
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