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• W2023721918 endingPage "428" @default.
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• W2023721918 abstract "CD4-unhelped CD8(+) T cells are functionally defective T cells primed in the absence of CD4(+) T cell help. Given the co-stimulatory role of natural-killer group 2, member D protein (NKG2D) on CD8(+) T cells, we investigated its ability to rescue these immunologically impotent cells. We demonstrate that augmented co-stimulation through NKG2D during priming paradoxically rescues memory, but not effector, CD8(+) T cell responses. NKG2D-mediated rescue is characterized by reversal of elevated transcription factor T-box expressed in T cells (T-bet) expression and recovery of interleukin-2 and interferon-γ production and cytolytic responses. Rescue is abrogated in CD8(+) T cells lacking NKG2D. Augmented co-stimulation through NKG2D confers a high rate of survival to mice lacking CD4(+) T cells in a CD4-dependent influenza model and rescues HIV-specific CD8(+) T cell responses from CD4-deficient HIV-positive donors. These findings demonstrate that augmented co-stimulation through NKG2D is effective in rescuing CD4-unhelped CD8(+) T cells from their pathophysiological fate and may provide therapeutic benefits." @default.
• W2023721918 created "2016-06-24" @default.
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• W2023721918 creator A5088420409 @default.
• W2023721918 date "2012-02-26" @default.
• W2023721918 modified "2023-09-30" @default.
• W2023721918 title "NKG2D signaling on CD8+ T cells represses T-bet and rescues CD4-unhelped CD8+ T cell memory recall but not effector responses" @default.
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• W2023721918 doi "https://doi.org/10.1038/nm.2683" @default.
• W2023721918 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3436127" @default.
• W2023721918 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22366950" @default.
• W2023721918 hasPublicationYear "2012" @default.
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