Bcl-2 increases memory B cell recruitment but does not perturb selection in germinal centers.

To address the role of apoptosis in the humoral immune response, we have examined a well-characterized T cell-dependent B cell response in mice expressing transgenic Bcl-2 in their B lymphocytes. The selection of somatic mutants and the appearance of high affinity antibodies was not affected by constitutive Bcl-2 expression. Such expression did, however, disproportionately increase the antigen-specific memory B cell pool, suggesting that the final size of the memory compartment may be regulated by an apoptotic process, which, in turn, can be influenced by Bcl-2. In addition, transgenic mice showed prolonged survival of foci of early antibody-producing cells, suggesting their removal is mediated by apoptosis that can be blocked by Bcl-2.