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- W4313385455 abstract "Abstract Efficient T cell immune activation requires a synergistic interaction between innate immune-derived reactive oxygen species (ROS) and pro-inflammatory cytokines. Our laboratory previously demonstrated that in the absence of NADPH oxidase (NOX)-derived superoxide, autoreactive T cell responses were profoundly compromised. To examine the role of ROS deficiency on antigen-specific T cells in a non-autoimmune setting and further test the hypothesis that Th1 T cell responses would be diminished in the absence of ROS, we generated the OT-II.Ncf1m1J mouse containing superoxide-deficient, OVA323-339-specific CD4 T cells. Stimulation of OT-II.Ncf1m1J elicited a 4-fold decrease in IFN-γ (p<0.05), concomitant with 2-fold reductions in CD4 T cell-derived IL-12Rβ2 and T-bet, required for Th1 activation. Th1 responses elicited by OVA323-339 stimulation were redox-sensitive, as addition of exogenous superoxide to OT-II.Ncf1m1J CD4 T cells restored IFN-γ synthesis and IL-12 signaling to approximately OT-II CD4 T cell levels. Conversely, Th1 responses were curbed in wild type OT-II T cells via free radical dissipation with a superoxide dismutase mimetic. This data highlights the importance of NOX-derived ROS in providing a third signal for adaptive immune maturation by modulating IL-12 signaling and may represent a promising therapeutic strategy in curbing CD4 T cell autoreactivity." @default.
- W4313385455 created "2023-01-06" @default.
- W4313385455 creator A5055845328 @default.
- W4313385455 creator A5060109722 @default.
- W4313385455 date "2016-05-01" @default.
- W4313385455 modified "2023-09-27" @default.
- W4313385455 title "NADPH oxidase-derived superoxide provides a third signal for CD4 T cell effector responses" @default.
- W4313385455 doi "https://doi.org/10.4049/jimmunol.196.supp.202.19" @default.
- W4313385455 hasPublicationYear "2016" @default.
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