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- W4313373553 abstract "Abstract We previously identified PSGL-1 (P-selectin glycoprotein-1) as a T cell-intrinsic, cell surface checkpoint inhibitor during chronic viral infection. In this model, we found that cross-linking PSGL-1 with antibody reduced signaling through the T cell receptor (TCR) in exhausted T cells and further upregulated PD-1 expression. However, the mechanism responsible for PD-1 regulation by PSGL-1 remained to be described. Here we show that, in naïve T cells, PSGL-1 ligation results in enhanced PD-1 expression following activation through the T cell receptor. Furthermore, naïve T cells lacking PSGL-1 fail to upregulate PD-1 to the same extent as wild type T cells following activation. Strikingly we have discovered that T cells lacking PSGL-1 showed reduced calcium signaling. In T cells, the calcium/calcineurin/NFAT pathway is important for induction of many genes including PD-1. Consequently, PSGL-1 deficient T cells also exhibit reduced nuclear translocation of NFAT explaining the reduced PD-1 expression. Conversely, we found that ligating PSGL-1 enhanced NFAT nuclear translocation with TCR signaling thus contributing to upregulation of PD-1. Therefore, by regulating calcium signaling through the T cell receptor, PSGL-1 modulates the extent of PD-1 expression early in activation and subsequently influencing the extent of T cell exhaustion. Further studies aim to elucidate how PSGL-1 regulates calcium signaling through the T cell receptor." @default.
- W4313373553 created "2023-01-06" @default.
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- W4313373553 date "2020-05-01" @default.
- W4313373553 modified "2023-09-27" @default.
- W4313373553 title "PSGL-1-directed regulation of calcium signaling modulates PD-1 expression following T cell activation" @default.
- W4313373553 doi "https://doi.org/10.4049/jimmunol.204.supp.80.19" @default.
- W4313373553 hasPublicationYear "2020" @default.
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