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Apoptosis and its modulation during B lymphopoiesis in mouse bone marrow

Summary: Studies in normal, gene‐deleted, transgenic and mutant mice have examined apoptotic cell death and its role in B lymphopoiesis in bone marrow. Apoptotic activity has been quantitated among phenotypically defined populations of precursor B cells using flow cytometry of apoptotic cells and an established model of B‐cell development. In normal mice, the frequencies of apoptotic cells (apoptotic index) and accumulation of apoptotic cells during short‐term culture (apoptotic rate) are maximal at around the pro/pre‐B‐cell transition and among immature B lymphocytes. The brief period between onset of apoptosis and clearance by macrophages (apoptotic transit time) is similar for most precursor B‐cells. Apoptosis‐modulating factors produce substantial changes in apoptotic activity among pro‐B and pre‐B cells, associated with altered expression of bcl‐2 family proteins. Pro‐B‐cell apoptosis, normally extensive, is markedly suppressed in the absence of p53. Complete pro‐B‐cell abortion in RAG‐2 deletion provides an assay for apoptotic fractions in other experimental systems. Pre‐B‐cell apoptosis is enhanced by deficiencies of interleukin (IL)‐7, Abl protooncogene or colony‐stimulating factor (CSF)‐1 and overexpression of heat‐stable antigen, and is inhibited by IL‐7 and p190bcr/abl transgenes. CSF‐1 and melatonin administration inhibit pre‐B‐cell apoptosis, probably via stromal cell stimulation. Such apoptotic modulation has implications for B‐cell homeostasis, quality control, immunodeficiency and neoplasia.