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B7-2 Regulates Survival, Phenotype, and Function of APCs¹

Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037

The absence of B7-2-mediated costimulation protects NOD mice from the development of diabetes. Although the effects of B7-2 on T cell priming are well known, its impact on the function of APCs is not fully elucidated. We tested APC function and survival in mice lacking B7-2. A significant reduction in the phagocytic ability was observed in both splenic and pancreatic lymph node-associated dendritic cells (DCs) in B7-2 knockout (KO) mice. DCs from B7-2KO mice exhibited enhanced susceptibility to death, which was reflected by their reduced total cell numbers. Phenotypic analysis of APCs in B7-2KO mice revealed a significantly decreased proportion of CD8⁺CD205⁺ DCs. Interestingly, an enhanced proportion of B7-H1⁺ and B7-DC⁺ DCs were observed in B7-2KO mice. Lastly, we found that B7-2 deficiency significantly diminished the PKC- response in APCs upon CD28-Ig stimulation. In conclusion our data suggests that B7-2 promotes the generation of a mature APC repertoire and promotes APC function and survival.

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 Grant AI064325 from the National Institutes of Health (to N.S.). D.Y. is the recipient of postdoctoral fellowship awards from Myasthenia Gravis Foundation of America and Juvenile Diabetes Research Foundation International.

² Address correspondence and reprint requests to Dr. Nora Sarvetnick, Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, Mail Drop IMM-23, La Jolla, CA 92037. E-mail address: noras{at}scripps.edu

³ Abbreviations used in this paper: DC, dendritic cell; PLN, pancreatic lymph node, KO, knockout; PKC, protein kinase C.