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1
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* Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322;
Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden; and
Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden
During the non-Ag-specific early phase of infection, IFN-
is believed to be primarily provided by NK and NKT cells in response to pathogen-derived inflammatory mediators. To test whether other cell types were involved in early IFN- release, IFN--producing cells were visualized in spleens and lymph nodes of LPS-injected mice. In addition to NK and NKT cells, IFN- was also detected in a significant fraction of CD8+ T cells. CD8+ T cells represented the second major population of IFN--producing cells in the spleen (
30%) and the majority of IFN-+ cells in the lymph nodes (70%). LPS-induced IFN- production by CD8+ T cells was MHC class I independent and was restricted to CD44high (memory phenotype) cells. Experiments performed with C3H/HeJ (LPS-nonresponder) mice suggested that CD8+ T cells responded to LPS indirectly through macrophage/dendritic cell-derived IFN-
/
, IL-12, and IL-18. IFN- was also detected in memory CD8+ T cells from mice injected with type I IFN or with poly(I:C), a synthetic dsRNA that mimics early activation by RNA viruses. Taken together, these results suggest that in response to bacterial and viral products, memory T cells may contribute to innate immunity by providing an early non-Ag-specific source of IFN-.
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