Published online before print June 7, 2007

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Copyright © 2007 American Society for Investigative Pathology
American Journal of Pathology, doi:10.2353/ajpath.2007.061279

Accepted for publication April 27, 2007.

Article

CD19 Expression in B Cells Is Important for Suppression of Contact Hypersensitivity

Rei Watanabe^*, Manabu Fujimoto^*@, Nobuko Ishiura^*, Yoshihiro Kuwano^*, Hiroko Nakashima^*, Norihito Yazawa^*, Hitoshi Okochi, Shinichi Sato, Thomas F. Tedder^¶, and Kunihiko Tamaki^*

From the Department of Dermatology,* Faculty of Medicine, University of Tokyo, Tokyo, Japan; the Department of Regenerative Medicine, Research Institute, International Medical Center of Japan, Tokyo, Japan; the Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; the Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; and the Department of Immunology,^¶ Duke University Medical Center, Durham, North Carolina

^@ To whom correspondence should be addressed. E-mail: fujimoto-m{at}umin.ac.jp.

	Abstract

Contact hypersensitivity (CHS) is a cutaneous immune reaction mediated mainly by antigen-specific effector T cells and is regarded as a model for Th1/Tc1-mediated inflammation. However, recent reports have suggested pivotal roles of B cells in CHS. CD19 serves as a positive B-cell response regulator that defines signaling thresholds critical for B-cell responses. In the current study, we assessed the role of the B-cell-specific surface molecule CD19 on the development of CHS by examining CD19-deficient mice. Although CD19-deficient mice are hyposensitive to a variety of transmembrane signals, CD19 loss resulted in increased and prolonged reaction of CHS, suggesting an inhibitory role of CD19 expression in CHS. Sensitized lymph nodes and elicited ear lesions from CD19-deficient mice exhibited Th1/Tc1-shifted cytokine profile with increased interferon- expression and decreased interleukin-10 expression. Adoptive transfer experiments revealed that CD19 expression in recipient mice was required for optimal suppression of CHS response, indicating its role in the elicitation phase. Furthermore, spleen B cells, especially marginal zone B cells, from wild-type mice were able to normalize exaggerated CHS reactions in CD19-deficient mice. Thus, CD19 expression in B cells is critical for termination of CHS responses, possibly through the function of regulatory B cells.