CD21 (complement receptor 2, CR2) binds the C3 degradation products, i
C3b and C3d, which are covalently linked to antigen or immune complexe
s in the process of complement activation. The ability of antigen-nons
pecific B cells to present immune complexes containing high titers of
acquired antibodies was tested. Influenza virus was incubated with ser
um from immune donors to create complement-containing complexes. These
bound specifically to CD21 on transfected fibroblasts and B cell line
s, as measured by microcytofluorimetry. Binding of immune complexes wa
s ablated by inactivation of serum complement. In addition, the immuno
globulin in immune human serum blocked influenza binding to cells in t
he absence of complement, implying a minimal role for immunoglobulin-F
c receptor interactions in this system. Significant immune complex bin
ding required a threshold level of CD21 expression, suggesting that on
ly those cells with the highest levels of CD21 are likely to participa
te in the processing of macromolecular antigens. B cells pulsed with c
omplement-influenza complexes elicited an augmented response from a pa
nel of influenza-specific, class II-restricted T cell clones, as compa
red with those which had bound immunoglobulin-influenza complexes lack
ing complement. This enhanced response did not require CD35. In additi
on, B cell lines expressing higher levels of CD21 were more efficient
in processing antigen than those with lower levels. These findings sug
gest that presentation of antigen by B cells in immune individuals is
dependent on the binding of complement-antigen immune complexes to CD2
1.