| First Author | Liang Y | Year | 2015 |
| Journal | Eur J Immunol | Volume | 45 |
| Issue | 11 | Pages | 3052-63 |
| PubMed ID | 26249267 | Mgi Jnum | J:233094 |
| Mgi Id | MGI:5780774 | Doi | 10.1002/eji.201545696 |
| Citation | Liang Y, et al. (2015) IL-33 promotes innate IFN-gamma production and modulates dendritic cell response in LCMV-induced hepatitis in mice. Eur J Immunol 45(11):3052-63 |
| abstractText | 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-gamma production in the liver. We first show that IL-33 deficiency resulted in a marked reduction in the number of IFN-gamma(+) gammadelta T and NK cells, but an increase in that of IL-17(+) gammadelta T cells at 16 h postinfection. Recombinant IL-33 (rIL-33) treatment could reverse such deficiency via increasing IFN-gamma-producing gammadelta T and NK cells, and inhibiting IL-17(+) gammadelta 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-gamma and TNF-alpha 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-gamma-production and DC function during viral hepatitis. |
