| First Author | Durbin JE | Year | 2000 |
| Journal | J Immunol | Volume | 164 |
| Issue | 8 | Pages | 4220-8 |
| PubMed ID | 10754318 | Mgi Jnum | J:123432 |
| Mgi Id | MGI:3718296 | Doi | 10.4049/jimmunol.164.8.4220 |
| Citation | Durbin JE, et al. (2000) Type I IFN modulates innate and specific antiviral immunity. J Immunol 164(8):4220-8 |
| abstractText | IFNs protect from virus infection by inducing an antiviral state and by modulating the immune response. Using mice deficient in multiple aspects of IFN signaling, we found that type I and type II IFN play distinct although complementing roles in the resolution of influenza viral disease. Both types of IFN influenced the profile of cytokines produced by T lymphocytes, with a significant bias toward Th2 differentiation occurring in the absence of responsiveness to either IFN. However, although a Th1 bias produced through inhibition of Th2 differentiation by IFN-gamma was not required to resolve infection, loss of type I IFN responsiveness led to exacerbated disease pathology characterized by granulocytic pulmonary inflammatory infiltrates. Responsiveness to type I IFN did not influence the generation of virus-specific cytotoxic lymphocytes or the rate of viral clearance, but induction of IL-10 and IL-15 in infected lungs through a type I IFN-dependent pathway correlated with a protective response to virus. Combined loss of both IFN pathways led to a severely polarized proinflammatory immune response and exacerbated disease. These results reveal an unexpected role for type I IFN in coordinating the host response to viral infection and controlling inflammation in the absence of a direct effect on virus replication. |
