Journal
JOURNAL OF IMMUNOLOGY
Volume 164, Issue 8, Pages 4220-4228Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.8.4220
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- NCI NIH HHS [CA16087] Funding Source: Medline
- NIAID NIH HHS [AI11823, AI28900] Funding Source: Medline
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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 HN, 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. The Journal of Immunology, 2000, 164: 4220-4228.
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