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,
* Department of Immunology and
Urological Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106
The magnitude and duration of CD8+ T cell-mediated responses in the skin to hapten sensitization and challenge, contact hypersensitivity (CHS), is negatively regulated by CD4+ T cells through an unknown mechanism. In this study we show that CD4+ T cells restrict the development and expansion of hapten-specific CD8+ T cells mediating CHS responses to 2,4-dinitrofluorobenzene. In the absence of CD4+ T cells, high numbers of hapten-specific CD8+ T cells producing IFN-
were detected in the skin-draining lymph nodes on day 5 postsensitization, and these numbers decreased slightly, but were maintained through day 9, correlating with the increased magnitude and duration of CHS responses observed in these mice. In the presence of CD4+ T cells, the number of hapten-specific CD8+ T cells producing IFN- detected on day 5 postsensitization was lower and quickly fell to background levels by day 7. The limited development of effector CD8+ T cells was associated with decreased numbers of hapten-presenting dendritic cells in the lymphoid priming site. This form of immunoregulation was absent after sensitization of Fas ligand-defective gld mice. Transfer of wild-type CD4+ T cells to gld mice restored the negative regulation of CD8+ T cell priming and the immune response to hapten challenge in gld-recipient mice. These results indicate that CD4+ T cells restrict hapten-specific CD8+ T cell priming for CHS responses through a Fas ligand-dependent mechanism.
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