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  Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel

Schmidt, M., Raghavan, B., Müller, V., Vogl, T., Fejer, G., Tchaptchet, S., et al. (2010). Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel. Nature Immunology, 11, 814-819.

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 Creators:
Schmidt, Marc, Author
Raghavan, Badrinarayanan, Author
Müller, Verena, Author
Vogl, Thomas, Author
Fejer, György1, Author              
Tchaptchet, Sandrine1, Author              
Keck, Simone2, Author              
Kalis, Christoph2, Author              
Nielsen, Peter J.3, Author              
Galanos, Chris2, Author              
Roth, Johannes, Author
Skerra, Arne, Author
Martin, Stefan, Author
Freudenberg, Marina A.1, Author              
Goebeler, Matthias, Author
Affiliations:
1Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
2Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              
3Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243645              

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 Abstract: Allergies to nickel (Ni2+) are the most frequent cause of contact hypersensitivity (CHS) in industrialized countries. The efficient development of CHS requires both a T lymphocyte-specific signal and a proinflammatory signal. Here we show that Ni2+ triggered an inflammatory response by directly activating human Toll-like receptor 4 (TLR4). Ni2+-induced TLR4 activation was species-specific, as mouse TLR4 could not generate this response. Studies with mutant TLR4 proteins revealed that the non-conserved histidines 456 and 458 of human TLR4 are required for activation by Ni2+ but not by the natural ligand lipopolysaccharide. Accordingly, transgenic expression of human TLR4 in TLR4-deficient mice allowed efficient sensitization to Ni2+ and elicitation of CHS. Our data implicate site-specific human TLR4 inhibition as a potential strategy for therapeutic intervention in CHS that would not affect vital immune responses.

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Language(s): eng - English
 Dates: 2010
 Publication Status: Published in print
 Pages: -
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 Rev. Type: Peer
 Identifiers: eDoc: 534676
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Title: Nature Immunology
  Alternative Title : Nat. Immunol.
Source Genre: Journal
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Pages: - Volume / Issue: 11 Sequence Number: - Start / End Page: 814 - 819 Identifier: -