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A more recent version of this article appeared on July 1, 2007

Published online before print April 5, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0207089

Received for publication February 2, 2007.
Revised March 19, 2007.
Accepted for publication March 19, 2007.

Article

Regulatory function of CD4+CD25+ T cells from Class II MHC-deficient mice in contact hypersensitivity responses

Danielle D. Kish *@, Anton V. Gorbachev *, and Robert L. Fairchild *{dagger}{ddagger}

*Department of Immunology and {dagger}Urological Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA; and {ddagger}Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA

@ To whom correspondence should be addressed. E-mail: kishd{at}ccf.org.


  Abstract

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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