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- W4313305977 abstract "Abstract We have previously shown that female transgenic mice expressing IFN-γ in the epidermis, under the control of the involucrin promoter, develop inflammatory skin disease and a form of murine lupus. To investigate the pathogenesis of this syndrome, we generated female IFN-γ transgenic mice congenitally deficient in either αβ or γδ T cells. TCRδ−/− transgenics continued to produce antinuclear autoantibodies and to develop severe kidney lesions. In contrast, TCRβ−/− IFN-γ transgenic mice failed to produce antinucleosome, anti-dsDNA, or antihistone autoantibodies, and kidney disease was abolished. Both αβ- and γδ-deficient transgenics continued to develop IFN-γ-associated skin disease, lymphadenopathy, and splenomegaly. The data show that the autoantibody-mediated pathology of murine lupus in IFN-γ transgenic mice is completely αβ T cell dependent and that γδ T cells cannot drive autoantibody production. These results imply that production of antinuclear autoantibodies in IFN-γ transgenic animals is Ag driven, and we identified clusters of apoptotic cells in the epidermis of the mice as a possible source of self Ags. Our findings emphasize the relevance of this murine lupus model to the human disease." @default.
- W4313305977 created "2023-01-06" @default.
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- W4313305977 date "1999-06-15" @default.
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- W4313305977 title "A Central Role for αβ T Cells in the Pathogenesis of Murine Lupus" @default.
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- W4313305977 doi "https://doi.org/10.4049/jimmunol.162.12.7241" @default.
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