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Published online before print July 6, 2005
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* Department of Immunology, Cleveland Clinic Foundation, Ohio; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio
1Correspondence: NB3-30, Department of Immunology, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195-0001. E-mail: kishd{at}ccf.org
Interleukin (IL)-2 functions to promote, as well as down-regulate, expansion of antigen-reactive CD4+ and CD8+ T cells, but the role of IL-2 in hapten-specific CD8+ T cell priming for contact hypersensitivity (CHS) responses remains untested. Using enzyme-linked immunospot to enumerate numbers of hapten-specific CD4+ and CD8+ T cells producing IL-2 in hapten-sensitized mice, the number of IL-2-producing CD8+ T cells was tenfold that of CD4+ T cells. Hapten-primed CD4+ T cells produced low amounts of IL-2 during culture with hapten-presenting Langerhans cells, whereas production by hapten-primed CD8+ T cells was fivefold greater. CD8+ T cells did not express CD25 during hapten priming, but treatment with anti-IL-2 or anti-CD25 monoclonal antibodies during hapten sensitization increased hapten-specific effector CD8+ T cells as well as the magnitude and duration of the CHS response. These results indicate that CD8+ T cells are the primary source of IL-2 and that this IL-2 is required for the function of a population of CD4+CD25+ T cells to restrict the development of the hapten-reactive effector CD8+ T cells that mediate CHS responses.
Key Words: delayed-type hypersensitivity T regulatory cells skin T cell priming
This article has been cited by other articles:
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D. D. Kish, A. V. Gorbachev, and R. L. Fairchild Regulatory function of CD4+CD25+ T cells from Class II MHC-deficient mice in contact hypersensitivity responses J. Leukoc. Biol., July 1, 2007; 82(1): 85 - 92. [Abstract] [Full Text] [PDF] |
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