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10.1038/s41467-018-05288-0

http://scihub22266oqcxt.onion/10.1038/s41467-018-05288-0
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C6045629!6045629!30006605
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suck abstract from ncbi


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pmid30006605      Nat+Commun 2018 ; 9 (ä): ä
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  • Nonstimulatory peptide?MHC enhances human T-cell antigen-specific responses by amplifying proximal TCR signaling #MMPMID30006605
  • Zhao X; Sankaran S; Yap J; Too CT; Ho ZZ; Dolton G; Legut M; Ren EC; Sewell AK; Bertoletti A; MacAry PA; Brzostek J; Gascoigne NRJ
  • Nat Commun 2018[]; 9 (ä): ä PMID30006605show ga
  • Foreign antigens are presented by antigen-presenting cells in the presence of abundant endogenous peptides that are nonstimulatory to the T cell. In mouse T cells, endogenous, nonstimulatory peptides have been shown to enhance responses to specific peptide antigens, a phenomenon termed coagonism. However, whether coagonism also occurs in human T cells is unclear, and the molecular mechanism of coagonism is still under debate since CD4 and CD8 coagonism requires different interactions. Here we show that the nonstimulatory, HIV-derived peptide GAG enhances a specific human cytotoxic T lymphocyte response to HBV-derived epitopes presented by HLA-A*02:01. Coagonism in human T cells requires the CD8 coreceptor, but not T-cell receptor (TCR) binding to the nonstimulatory peptide?MHC. Coagonists enhance the phosphorylation and recruitment of several molecules involved in the TCR-proximal signaling pathway, suggesting that coagonists promote T-cell responses to antigenic pMHC by amplifying TCR-proximal signaling.
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