VIRUS-SPECIFIC CD8(-5 PRODUCTION AND INDUCE AIRWAY EOSINOPHILIA() CELLS CAN SWITCH TO INTERLEUKIN)

Virus infections of the lung are thought to predispose individuals to asthma, a disease characterized by eosinophil infiltration of the airw ays. CD8(+) T cells are an important part of the host response to viru s infection, however, they have no reported role in eosinophil recruit ment. We developed a mouse model of virus peptide-stimulated CD8(+) T cell immune responses in the lung. We found that bystander CD4(+) T he lper cell type 2 immune responses to ovalbumin switched the virus pept ide-specific CD8(+) T cells in the lung to interleukin (IL) 5 producti on. Furthermore, when such IL-5-producing CD8 T cells were challenged via the airways with virus peptide, a significant eosinophil infiltrat ion was induced. In vitro studies indicated that IL-4 could switch the virus-specific CD8(+) T cells to IL-5 production. These results could explain the link between virus infection and acute exacerbation of as thma and, perhaps more importantly, they indicate an IL-4-dependent me chanism that would impair CD8(+) T cell responses and delay viral clea rance from the host.