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• W4297691837 endingPage "1599" @default.
• W4297691837 startingPage "1594" @default.
• W4297691837 abstract "Abstract Several recent studies have shown that dendritic cells (DC) pulsed with soluble proteins can present peptide epitopes derived from these exogenous antigens on major histocompatability complex (MHC) class I molecules and induce an antigen-specific cytotoxic T lymphocyte (CTL) response. We provide evidence here that DC use macropinocytosis to capture soluble antigens that are then presented on MHC class I molecules. The presentation of an epitope derived from soluble ovalbumin was transporter associated with antigen presentation (TAP)-dependent, brefeldin A-sensitive, blocked by inhibitors of proteasomes, and resistant to chloroquine. These data suggest that exogenous antigens access the cytosol of DC and are proccessed for presentation via the same pathway described for conventional MHC class I-restricted cytosolic antigens. Proinflammatory mediators such as tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) reduced the efficiency of ovalbumin presentation via this pathway. This reduced presentation was not due to impaired expression of class I molecules because these substances upregulated the cell surface expression of Kb-molecules comparable to levels induced by interferon-γ (IFN-γ) treatment. The addition of IFN-γ increased ovalbumin presentation even in the presence of TNF-α or LPS. These results show that DC might be involved in the cross-priming phenomenon. This could offer the immune system an additional pathway for effective priming of cytotoxic T cells and provide the possibility to activate both CD4 and CD8 T-cell responses." @default.
• W4297691837 created "2022-09-30" @default.
• W4297691837 creator A5014277422 @default.
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• W4297691837 date "1997-08-15" @default.
• W4297691837 modified "2023-10-13" @default.
• W4297691837 title "Presentation of Exogenous Protein Antigens on Major Histocompatability Complex Class I Molecules by Dendritic Cells: Pathway of Presentation and Regulation by Cytokines" @default.
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• W4297691837 doi "https://doi.org/10.1182/blood.v90.4.1594" @default.
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