Abstract

The third component of complement C3 has been found to control the entry of activated B cell blasts into the S-phase of the cell cycle (Erdei et al., 1985; Melchers et al., 1985). In its activity as a synergistic growth factor, it therefore replaces a-type B cell growth factors (BCGF; Corbel and Melchers, 1984) which have been found to act at the same temporal point (restriction point) in the cell cycle (Melchers and Lernhardt, 1985). Furthermore, soluble C3d inhibits the synergistic action of a-type BCGF (Melchers et al., 1985). These results have suggested that both C3 and a-type BCGF act by signalling through the C3d-specific complement receptor CR2 (Fearon, 1984). The growth regulating properties of the CR2 receptor for B cells have also been implied in studies which demonstrated stimulating activities of CR2-specific, monoclonal antibodies with human B cells (Nemerow et al, 1985). These results have prompted us to investigate whether a structural relationship exists between C3 and α-type BCGF.

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