Neutrophil Cytosolic Factor 1 in Dendritic Cells Promotes Autoreactive CD8⁺ T Cell Activation via Cross-Presentation in Type 1 Diabetes.

Aims: Reactive oxygen species are critical in driving the onset of type 1 diabetes (T1D). Ablation of derived from phagocytic NADPH oxidase 2 is protective against autoimmune diabetes in non-obese diabetic (NOD) mice. However, the mechanisms of NADPH oxidase 2-derived duanyu1670 in T1D pathogenesis need to be elucidated. Here, we have examined the role of Ncf1 (the regulatory subunit of NADPH oxidase 2) in dendritic cells (DC). Results:Ncf1-mutant DCs exhibit reduced ability to activate autoreactive CD8⁺ T cells despite no difference in co-stimulatory molecule expression or pro-inflammatory cytokine production. When provided with exogenous whole-protein antigen, Ncf1-mutant NOD DCs showed strong phagosome acidification and rapid antigen degradation, which lead to an absence of protein translocation into the cytoplasm and deficient antigenic peptide loading on MHC Class I molecules. Innovation: This study demonstrates that Ncf1 (p47^phox) is required for activation and effector function of CD8⁺ T cells by acting both intrinsically within the T cell as well as within professional antigen presenting cells. Conclusion: duanyu1670 promote CD8⁺ T cell activation by facilitating autoantigen cross-presentation by DCs. duanyu1670 scavengers could potentially represent an important component of therapies aiming to disrupt autoantigen presentation and activation of CD8⁺ T cells in individuals at-risk for developing T1D.

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