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• W2138815237 startingPage "5757" @default.
• W2138815237 abstract "Abstract Autoantigen administration via nasal mucosal tissue can induce systemic tolerance more effectively than oral administration in a number of experimental autoimmune diseases, including Ab-mediated experimental autoimmune myasthenia gravis, a murine model of myasthenia gravis. The mechanisms underlying nasal tolerance induction are not clear. In this study, we show that nasal administration of acetylcholine receptor (AChR) in C57BL/6 mice, before immunizations with AChR in adjuvant, results in delayed onset and reduced muscle weakness compared with control mice. The delayed onset and reduced muscle weakness were associated with decreased AChR-specific lymphocyte proliferation and decreased levels of anti-AChR Abs of the IgG2a and IgG2b isotypes in serum. The clinical and immunological changes in the AChR-pretreated C57BL/6 wild-type (wt) mice were comparable with those observed in AChR-pretreated CD8−/− mice, indicating that CD8+ T cells were not required for the generation of nasal tolerance. AChR-pretreated wt and CD8−/− mice showed augmented TGF-β and reduced IFN-γ responses, whereas levels of IL-4 were unaltered. Splenocytes from AChR-pretreated wt and CD8−/− mice, but not from CD4−/− mice, suppressed AChR-specific lymphocyte proliferation. This suppression could be blocked by Abs against TGF-β. Thus, our results demonstrate that the suppression induced in the present model is independent of CD8+ T cells and suggest the involvement of Ag-specific CD4+ Th3 cells producing TGF-β." @default.
• W2138815237 created "2016-06-24" @default.
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• W2138815237 date "1999-05-15" @default.
• W2138815237 modified "2023-10-14" @default.
• W2138815237 title "Mechanisms of Nasal Tolerance Induction in Experimental Autoimmune Myasthenia Gravis: Identification of Regulatory Cells" @default.
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• W2138815237 doi "https://doi.org/10.4049/jimmunol.162.10.5757" @default.
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