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10.4049/jimmunol.1202382

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C3700538!3700538!23636058
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suck abstract from ncbi


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pmid23636058      J+Immunol 2013 ; 190 (11): 5402-10
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  • Blockade of Programmed Death-1 (PD-1) in young (New Zealand Black × New Zealand White)F1 mice promotes the suppressive capacity of CD4+ regulatory T cells protecting from lupus-like disease #MMPMID23636058
  • Wong M; Cava AL; Hahn BH
  • J Immunol 2013[Jun]; 190 (11): 5402-10 PMID23636058show ga
  • PD-1 usually acts as a negative signal for T cell activation, and its expression on CD8+Foxp3+ T cells is required for their suppressive capacity. Here we show that PD-1 signalling is required for the maintenance of functional regulatory CD4+CD25+Foxp3+T cells (CD4+Treg) that can control autoimmunity in (New Zealand Black × New Zealand White) F1 (BWF1) lupus mice. PD-1 signalling induced resistance to apoptosis and prolonged the survival of CD4+Treg. In vivo, the blockade of PD-1 with a neutralizing antibody (Ab) reduced PD-1 expression on CD4+Treg (PD1loCD4+Treg). PD1loCD4+Treg had an increased ability to promote B cell apoptosis and to suppress CD4+ helper T cells (Th) as compared to CD4+Treg with elevated PD-1 expression (PD1hiCD4+Treg). When PD-1 expression on CD4+Treg was blocked in vitro, PD1loCD4+Treg suppressed B cell production of IgG and anti-dsDNA Ab. Finally, in vitro studies showed that the suppressive capacity of CD4+Treg depended on PD-1 expression, and that a fine tuning of the expression of this molecule directly affected cell survival and immune suppression. These results indicate that PD-1 expression has multiple effects on different immune cells that directly contribute to a modulation of autoimmune responses.
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