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10.4049/jimmunol.1700339

http://scihub22266oqcxt.onion/10.4049/jimmunol.1700339
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C5609833!5609833!28539427
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suck abstract from ncbi


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pmid28539427      J+Immunol 2017 ; 199 (1): 278-91
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  • Toll like receptor-induced murine dendritic cell activation requires dendritic cell-intrinsic complement #MMPMID28539427
  • Sheen JH; Strainic M; Lui J; Zhang W; Yi Z; Medof ME; Heeger PS
  • J Immunol 2017[Jul]; 199 (1): 278-91 PMID28539427show ga
  • Induction of pro-inflammatory T cell immunity is augmented by innate dendritic cell (DC) maturation commonly initiated by Toll-like receptor (TLR) signaling. We demonstrate that ligation of TLR3, 4, and 9 induces murine DC production of complement components and local production of the anaphylatoxin C5a. In vitro, ex vivo, and in vivo analyses show that TLR-induced DC maturation as assessed by surface phenotype, expression profiling by gene array, and functional ability to stimulate T cell responses, requires autocrine C3a- and C5a-receptor (C3ar1/C5ar1) signaling. Studies employing bone marrow chimeric animals and Foxp3-GFP/ERT2-Cre/dTomato fate mapping mice show that TLR-initiated, DC autocrine C3ar1/C5ar1 signaling causes expansion of effector T cells and instability of regulatory T cells and contributes T cell-dependent transplant rejection. Together, our data position immune cell-derived complement production and autocrine/paracrine C3ar1/C5ar1 signaling as crucial intermediary processes that link TLR-stimulation to DC maturation and the subsequent development of effector T cell responses.
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