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Adaptive Immunity against Listeria monocytogenes in the Absence of Type I Tumor Necrosis Factor Receptor p55
Journal article   Open access   Peer reviewed

Adaptive Immunity against Listeria monocytogenes in the Absence of Type I Tumor Necrosis Factor Receptor p55

Douglas W White, Vladimir P Badovinac, Xin Fan and John T Harty
Infection and immunity, Vol.68(8), pp.4470-4476
08/2000
DOI: 10.1128/IAI.68.8.4470-4476.2000
PMCID: PMC98351
PMID: 10899844
url
https://doi.org/10.1128/IAI.68.8.4470-4476.2000View
Published (Version of record) Open Access

Abstract

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.
Microbial Immunity and Vaccines

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