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Innate, antigen-independent role for T cells in the activation of the immune system by Propionibacterium acnes

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Tchaptchet,  Sandrine
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Kirberg,  Jörg
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Schamel,  Wolfgang W. A.
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Galanos,  Chris
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Freudenberg,  Marina A.
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Tchaptchet, S., Kirberg, J., Freudenberg, N., Schamel, W. W. A., Galanos, C., & Freudenberg, M. A. (2010). Innate, antigen-independent role for T cells in the activation of the immune system by Propionibacterium acnes. European Journal of Immunology, 40, 2506-2516.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-8EE4-5
Abstract
Propionibacterium acnes is a human commensal but also an opportunistic pathogen. In mice, P. acnes exerts strong immunomodulatory activities, including formation of intrahepatic granulomas and induction of LPS hypersensitivity. These activities are dependent on P. acnes recognition via TLR9 and subsequent IL-12-mediated IFN-γ production. We show that P. acnes elicits IL-12p40 and p35 mRNA expression in macrophages, and IFN-γ mRNA in liver CD4+ T cells and NK cells. After priming with P. acnes, CD4+ T cells serve as the major IFN-γ mRNA source. In the absence of CD4+ T cells, CD8+ T cells (regardless of antigenic specificity) or NK cells can produce sufficient IFN-γ to induce the P. acnes-driven immune effects. Moreover, in the absence of αβT cells, γδT cells also enable the development of strongly enhanced TNF-α and IFN-γ responses to LPS and intrahepatic granuloma formation. Thus, under microbial pressure, different T-cell types, independent of their antigen specificity, exert NK-cell-like functions, which contribute decisively to the activation of the innate immune system.