Antiviral immunity and the role of dendritic cells.
Using our experimental model we demonstrate the need for Th1 immune responses for recovery from influenza virus infection. Inoculation of IL-4 concurrent with infection significantly delays virus clearance and converts the immune response to a Th2 response. Immunization using live virus in the presence of IL-4 leads to generation of Th2 memory cells that fail to facilitate recovery upon subsequent virus infection. Inactivated virus expands Th2 cells, leading to responses similar to those observed following IL-4 infusion. Immunization using cultured dendritic cells incubated with live or inactivated virus mimics the results observed with direct virus injection. We demonstrate that in contrast to live virus-infected dendritic cells, inactivated virus fails to elicit Th1 immunity. This failure correlates with the inactivated viruses' inability to induce dendritic cell maturation. Thus, our data suggest that the polarity of the immune response is dictated by the nature of the antigen, and the trigger for influenza virus-induced DC maturation leading to Th1 immunity is dependent on virus replication.
López
Carolina B
CB
Department of Microbiology, Mount Sinai School of Medicine, New York University, New York, New York, USA.
Moran
Thomas M
TM
Schulman
Jerome L
JL
Fernandez-Sesma
Ana
A
D000818:Animals; D051379:Mice; D009975:Orthomyxoviridae / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*