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Elderly individuals have increased morbidity and mortality associated with infectious diseases due in part to the progressive age-associated decline in immune function. Despite this, the old mouse model ofMycobacterium tuberculosis infection has revealed a CD8- and gamma interferon (IFN-γ)-dependent early resistance to infection. In this study, we investigated the mechanism by which CD8 T cells from old mice contributed to the early immune response toM. tuberculosis . Following a low-dose aerosol infection withM. tuberculosis , CD8 T cells were identified as being a dominant source of IFN-γ expression in the lungs of old mice early after infection, before the typical onset of antigen-specific immunity. In addition,M. tuberculosis -induced IFN-γ production by CD8 T cells isolated from naïve old mice was major histocompatibility complex class I independent but was dependent on interleukin-12p70, confirming an innate role of CD8 T cells duringM. tuberculosis infection. Moreover, the ability of CD8 T cells from old mice to produce increased innate IFN-γ levels in response toM. tuberculosis infection was defined as a unique function of CD8 T cells from old mice and not the aged lung environment. Finally, we have identified increased expression of SET as being one possible mechanism by which CD8 T cells from old mice produce enhanced levels of IFN-γ. Additional characterizations of the signaling events that lead to enhanced innate IFN-γ production by CD8 T cells in old mice may lead to novel strategies to further enhance or perpetuate beneficial immune responses in the elderly.

infection and immunity

CD8 T Cells in Old Mice Contribute to the Innate Immune Response to<i>Mycobacterium tuberculosis</i>via Interleukin-12p70-Dependent and Antigen-Independent Production of Gamma Interferon

CD8 T Cells in Old Mice Contribute to the Innate Immune Response toMycobacterium tuberculosisvia Interleukin-12p70-Dependent and Antigen-Independent Production of Gamma Interferon