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Engagement of CD83 on B Cells Modulates B Cell Function In Vivo¹

Birte Kretschmer^*, Katja Lüthje^*, Stefanie Schneider^*, Bernhard Fleischer^*, and Minka Breloer^2,*

^* Department of Immunology, Bernhard-Nocht-Institute for Tropical Medicine, Hamburg, Germany; and Institute of Immunology, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany

The transmembrane glycoprotein CD83 is an important regulator of both thymic T cell maturation and peripheral T cell response. Recent studies suggested that CD83 is also involved in the regulation of B cell maturation, activation, and homeostasis. In this study, we show that in vivo overexpression of CD83 dose dependently interfered with the Ig response to thymus-dependent and thymus-independent model Ag immunization. CD83 deficiency, in contrast, which was restricted to B cells in mixed bone marrow chimeras, led to unchanged or even slightly increased Ig responses. Strikingly, the engagement of CD83 that is naturally up-regulated on wild-type B cells by injection of anti-CD83 mAb in vivo induced a 100-fold increase in the IgG1 response to immunization. Kinetic analysis revealed that CD83 had to be engaged simultaneously or shortly after the B cell activation through injection of Ag, to modulate the IgG1 secretion. Furthermore, using mixed bone marrow chimeras in which either selectively the B cells or the dendritic cells were CD83 deficient, we demonstrate that anti-CD83 mAb mediated its biologic effect by engaging CD83 on B cells and not on CD11c⁺ dendritic cells. Taken together, we provide strong evidence that CD83 transduces regulatory signals into the very B cell on which it is expressed.

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 the Deutsche Forschungsgemeinschaft (FL 129/5-1, 5-2).

² Address correspondence and reprint requests to Dr. Minka Breloer, Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Str. 74, D-20359 Hamburg, Germany.

³ Abbreviations used in this paper: DC, dendritic cell; DT, diphtheria toxin; DTR, DT receptor; mu, mutant; NIP, 4-hydroxy-3-iodo-5-nitrophenylacetyl; TD, thymus dependent; TEC, thymic epithelial cell; tg, transgenic; TI, thymus independent; f1, founder 1; f2, founder 2.

⁴ The online version of this article contains supplementary material.