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CD83 Expression Is a Sensitive Marker of Activation Required for B Cell and CD4⁺ T Cell Longevity In Vivo¹

Charlene M. Prazma^*, Norihito Yazawa^*, Yoko Fujimoto, Manabu Fujimoto and Thomas F. Tedder^2,*

^* Department of Immunology, Duke University Medical Center, Durham, NC 27710; Department of Neurology and Neurological Science, Tokyo Medical and Dental University, Tokyo, Japan; and Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan

CD83 is a surface marker that differentiates immature and mature human dendritic cell populations. Thymic epithelial cell expression of CD83 is also necessary for efficient CD4⁺ T cell development in mice. The altered phenotypes of peripheral B and CD4⁺ T cells, and the reduction of peripheral CD4⁺ T cells in CD83^–/– mice, suggest additional functions for CD83. To assess this, a panel of mAbs was generated to characterize mouse CD83 expression by peripheral leukocytes. As in humans, activation of conventional and plasmacytoid murine dendritic cell subsets led to rapid up-regulation of CD83 surface expression in mice. In primary and secondary lymphoid compartments, a subset of B cells expressed low-level CD83, while CD83 was not detected on resting T cells. However, CD83 was prominently up-regulated on the majority of spleen B and T cells within hours of activation in vitro. In vivo, a low dose of hen egg lysozyme (1 µg) induced significant CD83 but not CD69 expression by Ag-specific B cells within 4 h of Ag challenge. Although B cell development appeared normal in CD83^–/– mice, B and CD4⁺ T cell expression of CD83 was required for lymphocyte longevity in adoptive transfer experiments. Thus, the restricted expression pattern of CD83, its rapid induction following B cell and T cell activation, and its requirement for B cell and CD4⁺ T cell longevity demonstrate that CD83 is a functionally significant and sensitive marker of early lymphocyte activation in vivo.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants CA098492, CA96547, CA105001, and AI56363.

² Address correspondence and reprint requests to Dr. Thomas F. Tedder, Department of Immunology, Duke University Medical Center, Box 3010, Room 353 Jones Building, Research Drive, Durham, NC 27710. E-mail address: thomas.tedder{at}duke.edu

³ Abbreviations used in this paper: DC, dendritic cell; MHC II, MHC class II; cDC, conventional DC; pDC, plasmacytoid DC; HEL, hen egg lysozyme; NP, (4-hydroxy-3-nitrophenyl) acetate; CGG, chicken gammaglobulin; NZB/NZW, New Zealand Black/New Zealand White; PLN, peripheral lymph node.

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