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: Role of Stromal Cell Complement and FcRIIB Receptors

Robert A. Barrington¹, Olga Pozdnyakova¹, Mohammad R. Zafari², Christopher D. Benjamin² and Michael C. Carroll¹

¹ Center for Blood Research and Department of Pathology, Harvard University, Boston, MA 02115
² Biogen Inc., Cambridge, MA 02142

Address correspondence to Michael C. Carroll, Center for Blood Research, Harvard Medical School, LMRC 502, 221 Longwood Avenue, Boston, MA 02115. Phone: 617-432-1991; Fax: 617-432-2108; E-mail: mcarroll{at}cbr.med.harvard.edu

To dissect the influence of CD21/CD35 and FcRIIB in antigen retention and humoral memory, we used an adoptive transfer model in which antigen-primed B and T lymphocytes were given to sublethally irradiated wild-type mice or mice deficient in CD21/CD35 (Cr2^-/-) or FcRIIB receptors (FcRIIB^-/-). Cr2^-/- chimeras showed impaired memory as characterized by a decrease in antibody titer, reduced frequency of antibody secreting cells, an absence of affinity maturation, and significantly reduced recall response. The impaired memory in Cr2^-/- chimeras corresponded with the reduced frequency of antigen-specific memory B cells. Interestingly, FcRIIB^-/- chimeras showed a differential phenotype with impaired splenic but normal bone marrow responses. These data suggest that CD21/CD35 on stroma, including follicular dendritic cells, is critical to the maintenance of long-term B lymphocyte memory.

Key Words: B lymphocytes • memory • complement receptors • FcRIIB • follicular dendritic cells

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