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Fas-Mediated Inhibition of CD4⁺ T Cell Priming Results in Dominance of Type 1 CD8⁺ T Cells in the Immune Response to the Contact Sensitizer Trinitrophenyl¹

Stefan F. Martin^2,*, Jan C. Dudda^*, Virginie Delattre^*, Eva Bachtanian^*, Cornelia Leicht^*, Beate Burger^*, Hans Ulrich Weltzien and Jan C. Simon^*

^* Clinical Research Group Allergology, Department of Dermatology, University of Freiburg; and Max Planck Institute for Immunobiology, Freiburg, Germany

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.

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