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Fas-Mediated Ihhibition of CD4+ T Cell Priming Results in Dominance of Type 1 CD8+ T cells in the Immune Response to the Contact Sensitizer Trinitrophenyl

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Weltzien,  Hans-Ulrich
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Martin, S. F., Dudda, J. C., Delattre, V., Bachtanian, E., Leicht, C., Burger, B., et al. (2004). Fas-Mediated Ihhibition of CD4+ T Cell Priming Results in Dominance of Type 1 CD8+ T cells in the Immune Response to the Contact Sensitizer Trinitrophenyl. Journal of Immunology, 173, 3178-3185.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9483-E
Abstract
One of the unusual properties of chemically reactive haptens is their capacity to simultaneously generate immunogenic determinants for hapten-specific CD8+ and CD4+ T cells. Surprisingly, however, a clear dominance of CD8+ effector T cells is observed in murine contact hypersensitivity to various haptens and upon T cell priming with hapten-modified APCs in vitro. In this study we show that trinitrophenyl-specific CD8+ T cells actively prevent CD4+ T cell priming in vitro. This process requires cell-cell contact and is dependent on the expression of Fas on the CD4+ T cells. Our results reveal an important Fas-dependent mechanism for the regulation of hapten-specific CD4+ T cell responses by CD8+ T cells, which causes the dominance of CD8+ effector T cells and the active suppression of a CD4+ T cell response. Moreover, our demonstration of reduced contact hypersensitivity to trinitrophenyl in the absence of Fas, but not of perforin and/or granzymes A and B, underlines the important role of Fas as a pathogenetic factor for contact hypersensitivity.