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  Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity

Martin, S. F., Dudda, J. C., Bachtanian, E., Lembo, A., Liller, S., Dürr, C., et al. (2008). Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity. Journal of Experimental Medicine, 205, 2151-2162.

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 Creators:
Martin, Stefan F., Author
Dudda, Jan C., Author
Bachtanian, Eva, Author
Lembo, Annalisa1, Author              
Liller, Stefanie, Author
Dürr, Christoph, Author
Heimesaat, Markus, Author
Bereswill, Stefan, Author
Fejer, György2, Author              
Vassileva, Ralitsa2, Author              
Jakob, Thilo, Author
Freudenberg, Nikolaus, Author
Termeer, Christian, Author
Johner, Caroline3, Author              
Galanos, Chris1, Author              
Freudenberg, Marina A.2, Author              
Affiliations:
1Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              
2Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
3Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243640              

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 Abstract: Allergic contact hypersensitivity (CHS) is a T cell-mediated inflammatory skin disease. Interleukin (IL)-12 is considered to be important in the generation of the allergen-specific T cell response. Loss of IL-12 function in IL-12Rβ2-deficient mice, however, did not ameliorate the allergic immune response, suggesting alternate IL-12-independent pathways in the induction of CHS. Because exposure to contact allergens always takes place in the presence of microbial skin flora, we investigated the potential role of Toll-like receptors (TLRs) in the induction of CHS. Using mice deficient in TLR4, the receptor for bacterial lipopolysaccharide (LPS), IL-12 receptor (R) β2, or both, we show that the concomitant absence of TLR4 and IL-12Rβ2, but not the absence of TLR4 or IL-12Rβ2 alone, prevented DC-mediated sensitization, generation of effector T cells, and the subsequent CHS response to 2,4,6-trinitro-1-chlorobenzene (TNCB), oxazolone, and fluorescein isothiocyanate. Introduction of the TLR4 transgene into the TLR4/IL-12Rβ2 mutant restored the CHS inducibility, showing a requirement for TLR4 in IL-12-independent CHS induction. Furthermore, the concomitant absence of TLR2 and TLR4 prevented the induction of CHS to TNCB in IL-12-competent mice. Finally, CHS was inducible in germ-free wild-type and IL-12Rβ2-deficient mice, but not in germ-free TLR4/IL-12Rβ2 double deficient mice, suggesting that the necessary TLR activation may proceed via endogenous ligands.

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Language(s): eng - English
 Dates: 2008-08-25
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: eDoc: 400825
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Title: Journal of Experimental Medicine
  Alternative Title : JEM
Source Genre: Journal
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Pages: - Volume / Issue: 205 Sequence Number: - Start / End Page: 2151 - 2162 Identifier: -