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Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2013 ; 190 (11): 5402-10 Nephropedia Template TP
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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.