Exogenous interleukin 7 as a proliferative stimulant of early precursor B cells in mouse bone marrow: efficacy of IL-7 injection, IL-7 infusion and IL-7-anti-IL-7 antibody complexes.

B lymphocyte development in mouse bone marrow (BM) occurs in association with stromal cells which provide essential growth factors, notably interleukin 7 (IL-7). The ability of recombinant IL-7 given systemically by several modes of administration to stimulate proliferation of precursor B cells at successive stages of development was examined. Using immunofluorescence labelling and mitotic arrest, the in vivo proliferative cell dynamics of phenotypically defined B lineage cells was quantitated.

Prelymphomatous B cell hyperplasia in the bone marrow of interleukin-7 transgenic mice: precursor B cell dynamics, microenvironmental organization and osteolysis.

Transgenic mice carrying mouse interleukin-7 (IL-7) cDNA under the control of MHC class II (E alpha) promoter develop B lymphoid tumors. We have analyzed population dynamics of early precursor B cells and electron microscopic organization of bone marrow (BM) during the prelymphomatous phase. Immunofluorescence labeling of terminal deoxynucleotidyl transferase (TdT), B220 glycoprotein, and mu heavy chains have been used to quantitate three populations of pro-B cells lacking mu chains, cytoplasmic mu-bearing pre-B cells, and surface mu-bearing B lymphocytes.

Apoptosis and macrophage-mediated cell deletion in the regulation of B lymphopoiesis in mouse bone marrow.

Studies of cell population dynamics and microenvironmental organization of B lymphopoiesis in the bone marrow of normal mice and in various genetically modified states have shown that cell loss, involving processes of apoptosis and macrophage-mediated cell deletion, is a prominent feature of the primary genesis of B lymphocytes. Balanced against the influence of proliferative stimulants, the programmed death of precursor B cells provides a quantitative control, determining the magnitude of the final output of functional B lymphocytes to the peripheral immune system. The cell loss mechanisms can be readily set in motion by external or systemic influences, making the B-cell output particularly vulnerable to suppression by ionizing irradiation, stress or other systemic mediators.