Adaptive Immunity againstListeria monocytogenesin the Absence of Type I Tumor Necrosis Factor Receptor p55

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Abstract
Tumor necrosis factor (TNF) and the type I TNF receptor (TNFRI), p55, are critical for resistance against primary infections with the intracellular bacterial pathogenListeria monocytogenes. Importantly, however, susceptibility to primary listeriosis in cytokine-deficient mice does not preclude the development or expression of effective adaptive immunity against virulentL. monocytogenes. We used TNFRI−/−mice to study adaptive antilisterial immunity in the absence of interactions between TNF and TNFRI. Our experiments indicate that TNFRI−/−mice survive and clear high-dose challenges with an attenuated strain ofL. monocytogenesthat is incapable of cell-to-cell spread. Furthermore, TNFRI−/−mice immunized with attenuatedL. monocytogenesgo on to develop potent adaptive immunity to subsequent high-dose challenges with virulentL. monocytogenes. Interestingly, CD8+T-cell depletion in vivo inhibits immunity toL. monocytogenesin the spleen but not in the liver of TNFRI−/−mice. The adaptive immune response in these animals is characterized by activation of listeriolysin O-specific CD8+T cells, which are capable of transferring antilisterial immunity to naive wild-type C57BL/6 host mice. These experiments demonstrate the development and expression of potent CD8+T-cell-mediated antilisterial immunity in the absence of TNFRI.