Investigating the requirement of IL-17A and IFNg in EAE disease development using HLA-DR3.IL-17A −/−.IFNg −/−transgenic mice
نویسندگان
چکیده
Abstract Multiple sclerosis (MS), an autoimmune disease of the central nervous system, is thought to be mediated by autoreactive CD4+ T cells producing IL-17A and IFNg. However, it unclear if these cytokines are essential for development, progression, or both. We have shown that neither IFNg nor IL-17A, alone, required development in experimental encephalomyelitis (EAE), a mouse model MS, but absence either results different phenotypes. Specifically, HLA-DR3(DRB1*0301) (DR3).IFNg−/− mice develop severe atypical EAE characterized increased levels while DR3.IL-17A−/− mild, classical EAE. These data suggest may compensatory roles. To further investigate roles EAE, we generated HLA-DR3.IFNg−/−.IL-17A−/− double knockout (DKO) their immune profiles, gut microbiomes, phenotype. Our show DKO harbor distinct myeloid cell myelin antigen-specific responses, microbiota. Interestingly, mimicking phenotype IFNg−/− mice. Thus, our factors other than mediate susceptibility. Further characterizations ongoing better define precise pathology MS/EAE. NIAID/NIH (1R01AI137075-01) generous gift from Margaret Heppelmann Michael Wacek.
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ژورنال
عنوان ژورنال: Journal of Immunology
سال: 2023
ISSN: ['1550-6606', '0022-1767']
DOI: https://doi.org/10.4049/jimmunol.210.supp.170.04