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- Title
Deficient Contact Hypersensitivity Reaction in CD4−/− Mice Is Because of Impaired Hapten-Specific CD8+ T Cell Functions.
- Authors
Saint-Mezard, Pierre; Chavagnac, Cyril; Vocanson, Marc; Kehren, Jeanne; Rozières, Aurore; Bosset, Sophie; Ionescu, Marius; Dubois, Bertrand; Kaiserlian, Dominique; Nicolas, Jean-Francois; Beacute;rard, Frédeacute;ric
- Abstract
Mice deficient in the CD4 molecule (CD4−/−) are widely used to evaluate the requirement for CD4+ T cell help in viral, tumoral, and transplantation immunity. Previous studies, showing that CD4−/− mice develop impaired contact hypersensitivity (CHS) responses, have suggested that CD4+ T cells are required for the optimal induction of this skin inflammatory reaction. other studies have, however, demonstrated that CHS was mediated by CD8+ T cells, without the need for CD4+ T cell help. Here, we show that CD4−/− mice develop a normal delayed-type hypersensitivity response to protein antigen, which is mediated by major histocompatibility molecules class II-restricted CD4−CD8− T cells, but a decreased CHS response to 2,4-dinitro-fluorobenezene. Analysis of the hapten-specific T cell pool demonstrates that priming of CD8+ T cells occurred normally in CD4−/− mice, as assessed by specific proliferative responses and interferon-γ (IFN-γ) production of purified CD8+ T cells. Furthermore, CD8+ T cells were able to adoptively transfer a normal CHS reaction. In contrast, total lymph node cells from CD4−/− mice showed decreased IFN-γ production and diminished specific cytotoxic T lymphocytes (CTL) activity, which could be reversed byin vitrorestimulation with hapten-pulsed class II-deficient antigen-presenting cells. These data confirm that class I-restricted CD8+ T cells can fully develop in effectors of CHS in the absence of CD4+ T cell help and suggest that the impaired CHS in CD4−/− mice is because of the presence of a class II-restricted T cell subset, which controls CHS by inhibiting hapten-specific CTL responses.
- Subjects
CONTACT dermatitis; CD4 antigen; T cells; LYMPH nodes; MICE; TRANSPLANTATION immunology
- Publication
Journal of Investigative Dermatology, 2005, Vol 124, Issue 3, p562
- ISSN
0022-202X
- Publication type
Article
- DOI
10.1111/j.0022-202X.2005.23567.x