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- W4313355595 abstract "Abstract Persistent immune activation remains the hallmark of HIV infection even in the context of successfully suppressed viremia. Its clinical significance is suggested by increased risk to develop non-AIDS defining illnesses such as cardiovascular disease. We previously have shown that human CD4 and CD8 T cells with effector memory and terminal effector memory phenotype expressed the protease activated receptor-1 (PAR1) and that expression was increased in CD8 T cells from HIV infected patients. Thrombin, in a PAR1 dependent fashion, enhanced CD8 T cell function measured by increased secretion of IFN-g and chemokinesis. PAR1 is the main receptor of thrombin and is also expressed on platelets and endothelial cells suggesting a cross-talk between the coagulation system and T cells at the site of vascular injury. To address the role of PAR1 in vivo, we used an infection model with the hepatotropic strain of lymphocytic choriomeningitis virus (LCMV-WE). To evaluate the role of PAR1 signaling in this model, we analyzed the T cells of littermate wild type control and PAR1−/−mice eight days following infection with LCMV-WE (2×105 pfu i.v.). In this model, we observed a similar expansion of total CD8 T cells in the spleens and livers of both WT and PAR1−/−mice at 8 days post infection. Despite similar expansion, PAR1 deficient mice showed impaired viral clearance at day 8 of infection. This lack of viral control was associated with a significant reduction in cytokine secretion by gp-33-specific CD8 T cells in the livers and spleens. These results suggest that PAR1 deficiency leads to an impair viral control that is in part mediated by a decrease ability to secrete cytokine by virus specific CD8 T cells." @default.
- W4313355595 created "2023-01-06" @default.
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- W4313355595 date "2018-05-01" @default.
- W4313355595 modified "2023-09-23" @default.
- W4313355595 title "Protease activated receptor-1 signaling: its potential implication in HIV driven immune activation, inflammation/coagulation" @default.
- W4313355595 doi "https://doi.org/10.4049/jimmunol.200.supp.61.6" @default.
- W4313355595 hasPublicationYear "2018" @default.
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