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- W4313368462 abstract "Abstract Friend virus (FV) is a murine retroviral complex that establishes chronic infection characterized by the induction of CD4+Foxp3+ Tregs and prolonged exposure to antigenic stimulation. This leads to a state of diminished CD8+ T cell function, termed “exhaustion”, in the spleens of FV-infected mice. We report that during exhaustion there is a subset of functional CD8+ T cells defined by surface expression of signal regulatory protein alpha (SIRPα), whose expression had previously been reported on neurons, myeloid and hematopoietic stem cells but not T cells. This subset of SIRPα+ CD8+ T cells has high expression of multiple inhibitory receptors including PD-1, Tim3 and Fas, while maintaining high expression of activation/stimulatory molecules including ICOS and CD43. In addition, SIRPα+CD8+ T cells exhibit enhanced proliferation and maintain cytolytic capability, despite the conditions of exhaustion existing within the spleens of chronically infected mice. Furthermore, target cells that express the ligand for SIRPα, CD47, are more susceptible to CD8+ T cell-killing in vivo. We now demonstrate that SIRPα expression on CD8+ T cells is tissue specific, occurring in the spleen but not liver. This is interesting as we have previously reported that the liver has a 10-fold reduction of chronic FV levels, which correlates with reduced Treg-mediated suppression and increased CD8+ T cell function. Furthermore, the SIRPα− CD8+ T cells from the liver of chronically infected mice appear equivalently cytolytic to SIRPα+ CD8+ T cells from the spleen. Therefore, SIRPα expression identifies functional cytotoxic T cells in the spleen but not the liver during chronic exhaustion, highlighting tissue-specific differences of viral control." @default.
- W4313368462 created "2023-01-06" @default.
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- W4313368462 date "2020-05-01" @default.
- W4313368462 modified "2023-09-27" @default.
- W4313368462 title "Functional cytotoxic T cells exhibit tissue-specific phenotypic differences during chronic Friend virus infection" @default.
- W4313368462 doi "https://doi.org/10.4049/jimmunol.204.supp.94.3" @default.
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