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The discovery of CD5+ B cells by Hayakawa et al. (1) initiated a 13 year-long discussion about the origin and functional properties of these cells. The CD5+ B cells (B-1a) and their phenotypic CD5− “twins” (B-1b cells) differ from conventional peripheral B cells (B-2) by anatomical location, developmental origin, surface marker expression, antibody repertoire and growth properties (2–4). B-1 cells form a dominant population of B lineage cells in the peritoneal cavity, but are rare in the spleen and lymph nodes of adult mice (3–6). The progenitors of B-1a cells are abundant in the fetal omentum and liver but in contrast to the progenitors of conventional B-2 cells, are missing in the bone marrow of adult mice (3, 7–9). The progenitors of B-1b cells are present in the fetal omentum and liver as well as in the bone marrow of adult mice (10, 11). However, a supply of B-1b cells from the bone marrow appears to be restricted by a negative feedback mechanism according to which the entrance of newly generated cells into the adult peripheral pool of B-1 cells is prevented by the presence of the mature B-1 population (12). In the absence of a continuous supply of bone marrow–derived B-1 cells, the size of the B-1 cell population is kept constant due to the self-renewal capacity of B-1 cells (3, 13). Due to their ability to produce large quantities of multireactive IgM, IgG3 and IgA, B-1 cells are considered carriers of “natural immunity” (7). It seems that the maintenance of B-1 cell population at a stable level might be necessary to control the level of antibody production by these cells. Thus the anti– IL-10 antibody-induced ablation of B-1 cells is accompanied by a drastic reduction of serum immunoglobulin titers (14). On the other hand, the expansion of autoreactive B-1 cells is associated with the development of autoimmunity in mice and man (15).

Bar Mitzvah for B-1 Cells: How Will They Grow Up?