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- W4313355133 abstract "Abstract MyD88 is a critical component of most TLR signaling pathways. Earlier we demonstrated that MyD88-deficient (MyD88-/-) mice are hypersusceptible to infection by a vaccine strain (aroA-/aroD-) of Salmonella typhimurium (designated BRD509). Curiously, infected mice exhibited a state of hypergammaglobulinemia, with high levels of anti-Salmonella Abs of all IgG isotypes. The dysregulated Ab response also lead to production of anti-dsDNA and anti-thyroglobulin autoantibodies and immune complex deposition in kidneys. Increased susceptibility of MyD88-/- mice has been linked to poor type-1 cytokine responses. Therefore, we assessed the response of these mice to infection with a S. typhimurium engineered to express murine IFN-γ (GIDIFN). Infection studies using different doses of BRD509 and GIDIFN strains revealed that the latter strain was >100-fold less virulent in MyD88-/- mice than BRD509 and correlated with decreased bacterial loads in systemic organs and robust pathogen clearance starting at 7 days of infection. Although GIDIFN-infected mice exhibited high Ab titers, the degree of autoreactivity was significantly decreased compared to BRD509-infected animals. Our data suggest that TLR-MyD88 signaling pathway is critical for controlling Ab responses to bacterial antigens and for maintaining B cell self-tolerance and demonstrate that the two processes may be unlinked through the use of cytokine-expressing bacterial strains that modulate host immune responses." @default.
- W4313355133 created "2023-01-06" @default.
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- W4313355133 date "2013-05-01" @default.
- W4313355133 modified "2023-09-26" @default.
- W4313355133 title "Differential regulation of immune responses in MyD88-deficient mice by cytokine-expressing <i>Salmonella typhimurium</i> (P4046)" @default.
- W4313355133 doi "https://doi.org/10.4049/jimmunol.190.supp.44.8" @default.
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