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• W3001844385 abstract "Abstract Mucosal-associated invariant T (MAIT) cells acquire effector function in response to proinflammatory signals, which synergize with TCR-mediated signals. We asked if cell-intrinsic regulatory mechanisms exist to curtail MAIT cell effector function akin to the activation-induced expression of inhibitory receptors by conventional T cells. We examined human MAIT cells from blood and oral mucosal tissues by RNA sequencing and found differential expression of immunoregulatory genes, including CTLA-4, by MAIT cells isolated from tissue. Using an ex vivo experimental setup, we demonstrate that inflammatory cytokines were sufficient to induce CTLA-4 expression on the MAIT cell surface in the absence of TCR signals. Even brief exposure to the cytokines IL-12, IL-15, and IL-18 was sufficient for sustained CTLA-4 expression by MAIT cells. These data suggest that control of CTLA-4 expression is fundamentally different between MAIT cells and conventional T cells. We propose that this mechanism serves to limit MAIT cell–mediated tissue damage." @default.
• W3001844385 created "2020-01-30" @default.
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• W3001844385 date "2020-01-01" @default.
• W3001844385 modified "2023-10-02" @default.
• W3001844385 title "Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells" @default.
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• W3001844385 doi "https://doi.org/10.4049/immunohorizons.1900061" @default.
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