C3 activation and T-independent B cell stimulation

SOME highly polymerised immunogens with repeated antigenic determinants, such as bacterial polysaccharides or polymerised flagellin and hapten conjugates of these, can stimulate mouse B lymphocytes to make antibody without requiring the cooperative helper activity of T lymphocytes1. The mechanism whereby such T-independent immunogens, after interaction with the surface receptors on specifically responsive B lymphocytes, trigger these into activity is uncertain. Dukor and Hartmann2 have postulated that binding of activated C3 to complement receptors on B cells acts as a necessary second signal for antibody production. They envisage that T-independent antigens and B-cell mitogens generate this second signal by their ability to activate C3 through the ‘bypass’ pathway, whereas in the case of T-dependent antigens the signal derives from C3 cleavage by proteases released by activated T cells.