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• W1480050218 abstract "Recent studies have revealed IL-33 as a key factor in promoting antiviral T-cell responses. However, it is less clear as to how IL-33 regulates innate immunity. In this study, we infected wild-type (WT) and IL-33−/− mice with lymphocytic choriomeningitis virus and demonstrated an essential role of infection-induced IL-33 expression for robust innate IFN-γ production in the liver. We first show that IL-33 deficiency resulted in a marked reduction in the number of IFN-γ+ γδ T and NK cells, but an increase in that of IL-17+ γδ T cells at 16 h postinfection. Recombinant IL-33 (rIL-33) treatment could reverse such deficiency via increasing IFN-γ-producing γδ T and NK cells, and inhibiting IL-17+ γδ T cells. We also found that rIL-33-induced type 2 innate lymphoid cells were not involved in T-cell responses and liver injury, since the adoptive transfer of type 2 innate lymphoid cells neither affected the IFN-γ and TNF-α production in T cells, nor liver transferase levels in lymphocytic choriomeningitis virus infected mice. Interestingly, we found that while IL-33 was not required for costimulatory molecule expression, it was critical for DC proliferation and cytokine production. Together, this study highlights an essential role of IL-33 in regulating innate IFN-γ-production and DC function during viral hepatitis." @default.
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• W1480050218 date "2015-08-28" @default.
• W1480050218 modified "2023-09-24" @default.
• W1480050218 title "IL-33 promotes innate IFN-γ production and modulates dendritic cell response in LCMV-induced hepatitis in mice" @default.
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• W1480050218 doi "https://doi.org/10.1002/eji.201545696" @default.
• W1480050218 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4813322" @default.
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