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  T Cell Receptor Transfection Shows Non-HLA-Restricted Recognition of Nickel by CD8+ Human T Cells to be Mediated by αβ T Cell Receptors

Moulon, C., Choleva, Y., Thierse, H. J., Wild, D., & Weltzien, H.-U. (2003). T Cell Receptor Transfection Shows Non-HLA-Restricted Recognition of Nickel by CD8+ Human T Cells to be Mediated by αβ T Cell Receptors. Journal of Investigative Dermatology, 121(3), 496-501.

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 Creators:
Moulon, Corinne1, Author           
Choleva, Yoanna, Author
Thierse, Hermann J.2, Author           
Wild, Doris1, Author           
Weltzien, Hans-Ulrich1, Author           
Affiliations:
1Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              
2Research 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: CD8+ T cells have been assigned a prominent role in allergic contact dermatitis, including nickel allergy; however, human nickel-reactive T cells of the CD8+ phenotype have largely escaped detailed investigation. Here we characterize two quite unusual nickel-specific cytotoxic T cell clones isolated from the peripheral blood of two nickel-sensitized patients. These clones mediate nickel-specific cytolysis of many human cell lines, independent of the expression of HLA class I, CD1, or HLA class II molecules. Lysis is mediated by the αβ T cell receptors and involves the perforin, but not the Fas/Fas ligand pathway. Both antigen receptors lack sequence homology to each other as well as to typical natural killer T cell receptors. A transfectant expressing the rearranged αβ T cell receptor derived from one of the T cell clones unequivocally demonstrates that the T cell receptor itself is necessary and sufficient to confer HLA-independent nickel specificity. The independent isolation of these clones from two individuals points to an important role of such cells in the pathology of nickel contact dermatitis.

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Language(s): eng - English
 Dates: 2003-09
 Publication Status: Issued
 Pages: -
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 Table of Contents: -
 Rev. Type: -
 Identifiers: eDoc: 126506
ISI: 000185073800016
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Title: Journal of Investigative Dermatology
  Alternative Title : J. Invest. Dermatol.
Source Genre: Journal
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Pages: - Volume / Issue: 121 (3) Sequence Number: - Start / End Page: 496 - 501 Identifier: ISSN: 0022-202X