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- W1973186787 abstract "RATIONALE: Several studies have shown that in the absence of MyD88, Th1 responses are abrogated, but Th2 responses are still intact or augmented. Our lab, however, has shown that MyD88 is required for the induction of both TLR4 dependent Th1 and Th2 responses to inhaled antigen in a mouse model of asthma. Many studies have shown that regulatory T cells can suppress the functional maturation of DCs, therefore we sought to ask if regulatory T cells are involved in this unresponsiveness, and if so, what mechanism would be involved. METHODS: Regulatory T cells were depleted 3 days before sensitization. Mice were sensitization intranasally with LPS together with OVA for three days and then challenged with inhaled OVA on day 14, 15, 18 and 19. Mice were analyzed on day 21. IFN-β expression was analyzed with real-time PCR using RNA made from the mice primed with LPS for 2 hours. RESULTS: We showed that after the depletion of regulatory T cells, the Th2 responses to the inhaled antigens have been restored in the MyD88 deficient mice. We further showed that the TRIF pathway is defective in pulmonary DCs in the absence of MyD88. This is evidenced by the fact that LPS-induced IFNβ expression in MyD88-/- pulmonary DCs is absent in vivo. After depletion of regulatory T cells LPS-induced IFNβ expression is restored. CONCLUSIONS: Our researches suggests that naturally occurring regulatory T cells can influence pulmonary DCs maturation by inhibiting the TLR4-dependent TRIF signaling pathway." @default.
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- W1973186787 date "2007-01-01" @default.
- W1973186787 modified "2023-09-27" @default.
- W1973186787 title "CD4+CD25+ T cells Regulate TLR4 Signaling in Pulmonary Dendritic Cells" @default.
- W1973186787 doi "https://doi.org/10.1016/j.jaci.2006.12.576" @default.
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