Adaptive Immunity against Listeria monocytogenes in the Absence of Type I Tumor Necrosis Factor Receptor p55
AUTOR(ES)
White, Douglas W.
FONTE
American Society for Microbiology
RESUMO
Tumor necrosis factor (TNF) and the type I TNF receptor (TNFRI), p55, are critical for resistance against primary infections with the intracellular bacterial pathogen Listeria monocytogenes. Importantly, however, susceptibility to primary listeriosis in cytokine-deficient mice does not preclude the development or expression of effective adaptive immunity against virulent L. 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 of L. monocytogenes that is incapable of cell-to-cell spread. Furthermore, TNFRI−/− mice immunized with attenuated L. monocytogenes go on to develop potent adaptive immunity to subsequent high-dose challenges with virulent L. monocytogenes. Interestingly, CD8+ T-cell depletion in vivo inhibits immunity to L. monocytogenes in 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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=98351Documentos Relacionados
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