Journal
JOURNAL OF IMMUNOLOGY
Volume 177, Issue 10, Pages 7146-7154Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.10.7146
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Funding
- NCRR NIH HHS [P20 RR20171] Funding Source: Medline
- NIAID NIH HHS [AI055962] Funding Source: Medline
- NIDDK NIH HHS [DK34854] Funding Source: Medline
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IFN-gamma is critical for innate immunity against Listeria monocytogenes (L. monocytogenes), and it has long been thought that NK cells are the major source of IFN-gamma during the first few days of infection. However, it was recently shown that a significant number of CD44(high)CD8(+) T cells also secrete IFN-gamma in an Ag-independent fashion within 16 h of infection with L. monocytogenes. In this report, we showed that infection with other intracellular pathogens did not trigger this early IFN-gamma response and that cytosolic localization of Listeria was required to induce rapid IFN-gamma production by CD44(high)CD8(+) T cells. Infection of C57BL/6 mice with an Escherichia coli strain expressing listeriolysin O (LLO), a pore-forming toxin from L. monocytogenes, also resulted in rapid IFN-gamma expression by CD8(+) T cells. These results suggest that LLO expression is essential for induction of the early IFN-gamma response, although it is not yet clear whether LLO plays a direct role in triggering a signal cascade that leads to cytokine production or whether it is required simply to release other bacterial product(s) into the host cell cytosol. Interestingly, mouse strains that displayed a rapid CD8(+) T cell IFN-gamma response (C57BL/6, 129, and NZB) all had lower bacterial burdens in the liver 3 days postinfection compared with mouse strains that did not have an early CD8(+) T cell IFN-gamma response (BALB/c, A/J, and S/L). These data suggest that participation of memory CD8(+) T cells in the early immune response against L. monocytogenes correlates with innate host resistance to infection.
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