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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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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-002B-8EDA-0 Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-002B-8EDB-E
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Schmidt, Marc, Autor
Raghavan, Badrinarayanan, Autor
Müller, Verena, Autor
Vogl, Thomas, Autor
Fejer, György1, Autor           
Tchaptchet, Sandrine1, Autor           
Keck, Simone2, Autor           
Kalis, Christoph2, Autor           
Nielsen, Peter J.3, Autor           
Galanos, Chris2, Autor           
Roth, Johannes, Autor
Skerra, Arne, Autor
Martin, Stefan, Autor
Freudenberg, Marina A.1, Autor           
Goebeler, Matthias, Autor
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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 Zusammenfassung: 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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Sprache(n): eng - English
 Datum: 2010
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 534676
 Art des Abschluß: -

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Titel: Nature Immunology
  Alternativer Titel : Nat. Immunol.
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 11 Artikelnummer: - Start- / Endseite: 814 - 819 Identifikator: -