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  TLR9-Dependent and Independent Pathways Drive Activation of the Immune System by Propionibacterium Acnes

Tchaptchet, S., Gumenscheimer, M., Kalis, C., Freudenberg, N., Hölscher, C., Kirschning, C. J., et al. (2012). TLR9-Dependent and Independent Pathways Drive Activation of the Immune System by Propionibacterium Acnes. PLoS ONE, 7, e39155-e39155.

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 Creators:
Tchaptchet, Sandrine1, Author              
Gumenscheimer, Marina2, Author              
Kalis, Christoph3, Author              
Freudenberg, Nikolaus, Author
Hölscher, Christoph1, Author              
Kirschning, Carsten J., Author
Lamers, Marinus2, Author              
Galanos, Chris3, Author              
Freudenberg, Marina A.1, Author              
Affiliations:
1Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
2Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243654              
3Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              

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 Abstract: Propionibacterium acnes is usually a relatively harmless commensal. However, under certain, poorly understood conditions it is implicated in the etiology of specific inflammatory diseases. In mice, P. acnes exhibits strong immunomodulatory activity leading to splenomegaly, intrahepatic granuloma formation, hypersensitivity to TLR ligands and endogenous cytokines, and enhanced resistance to infection. All these activities reach a maximum one week after P. acnes priming and require IFN-γ and TLR9. We report here the existence of a markedly delayed (1-2 weeks), but phenotypically similar TLR9-independent immunomodulatory response to P. acnes. This alternative immunomodulation is also IFN-γ dependent and requires functional MyD88. From our experiments, a role for MyD88 in the IFN-γ-mediated P. acnes effects seems unlikely and the participation of the known MyD88-dependent receptors, including TLR5, Unc93B-dependent TLRs, IL-1R and IL-18R in the development of the alternative response has been excluded. However, the crucial role of MyD88 can partly be attributed to TLR2 and TLR4 involvement. Either of these two TLRs, activated by bacteria and/or endogenously generated ligands, can fulfill the required function. Our findings hint at an innate immune sensitizing mechanism, which is potentially operative in both infectious and sterile inflammatory disorders.

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Language(s): eng - English
 Dates: 2012-06
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: eDoc: 634476
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Title: PLoS ONE
Source Genre: Journal
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Pages: - Volume / Issue: 7 Sequence Number: - Start / End Page: e39155 - e39155 Identifier: -