Published online before print April 5, 2007
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* Department of Immunology and
Urological Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
1 Correspondence: NB3-30, Department of Immunology, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195-0001, USA. E-mail: kishd{at}ccf.org
Contact hypersensitivity (CHS) is a CD8+ T cell-mediated, inflammatory response to hapten sensitization and challenge of the skin. During sensitization, the magnitude and duration of hapten-specific CD8+ T cell expansion in the skin-draining lymph nodes (LN) are restricted by CD4+CD25+ T regulatory cells (Treg). The regulation of hapten-specific CD8+ T cell priming in Class II MHC-deficient (MHC/) mice was investigated. Although hapten-specific CD8+ T cell priming and CHS responses were elevated in Class II MHC/ versus wild-type mice, presensitization depletion of CD4+ or CD25+ cells in Class II MHC/ mice further increased CD8+ T cell priming and the elicited CHS response. Flow cytometry analyses of LN cells from Class II MHC/ mice revealed a population of CD4+ T cells with a majority expressing CD25. Forkhead box p3 mRNA was expressed in LN cells from Class II MHC/ and was reduced to background levels by depletion of CD4+ or CD25+ cells. Isolated CD4+CD25+ T cells from wild-type and Class II MHC/ mice limited in vitro proliferation of alloantigen- and hapten-specific T cells to antigen-presenting stimulator cells. These results identify functional CD4+CD25+ Treg in Class II MHC/ mice, which restrict hapten-specific CD8+ T cell priming and the magnitude of CHS responses.
Key Words: suppression Treg MHC/
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