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.
Smith
K G
KG
Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melborne Hospital, Victoria, Australia.
Weiss
U
U
Rajewsky
K
K
Nossal
G J
GJ
Tarlinton
D M
DM
D000818:Animals; D017209:Apoptosis / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D001483:Base Sequence; D006801:Humans; D007109:Immunity; D007156:Immunologic Memory; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D011518:Proto-Oncogene Proteins / Q000276:immunology* / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2; D013154:Spleen / Q000276:immunology / Q000473:pathology
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2