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Abstract
B cells are induced to antibody production by antigens or by mitogens, such as lipopolysaccharide (LPS). We observed a mutually antagonistic relationship between activation through the antigen-receptor (AgR) and LPS-receptor (LPSR) in vitro. Prior exposure of B cells to AgR-ligating antibody prevented antibody forming cell (AFC) production induced by LPS, but not that induced by specific antigen (SRBC, TNP-Ficoll, or TNP-LPS). AFC production induced by antigen could be abrogated by concomitant exposure to LPS; the shutdown of the antigen-driven response was apparent when LPS-induced AFC were prevented by pre-exposure to antibody against the AgR. The ability of signaling through the AgR to inhibit antibody production stimulated by LPS was seen in DBA/2 and BALB/c mouse strains, and not in the New Zealand Black (NZB) strain. The results suggest that mutual antagonism is distinct from other forms of immune hyporesponsiveness, and that defects in antagonism may be a factor in the development of autoimmune disease.