Studies of congenitally immunologic mutant New Zealand mice. III. Growth of B lymphocyte clones in congenitally athymic (nude) and hereditarily asplenic (Dh/+) NZB mice: A primary B cell defect

There is a growing data base suggesting the existence of a primary B cell defect in New Zealand mice. To identify and characterize this possibility further, attention has been focused on developmental aspects of B lymphocyte clone formation in congenitally athymic (nude), hereditarily asplenic (Dh/+), conventionally housed, and germfree New Zealand Black (NZB) mice. Lipopolysaccharide-induced and background B lymphocyte cloning of fetal liver, spleen, lymph node, bone marrow, and thymus in semisolid agar was compared in NZB mice to age-matched NZW, BALB/c, C57BL/6, C3H/He, and DBA/2N mice. The number of splenic B cell colony-forming cells and the peak day for colony formation were similar for BALB/c, C57BL/6, C3H/He, and DBA/2N mice; adult values were reached by 14 to 30 days and were approximately 400/2.5 x 10⁴ cells. A slightly higher value, with similar age kinetics, was observed in NZW mice. In contrast, NZB mice have statistically higher values compared to other strains from birth through 2 months of age; peak adult values were approximately 860/2.5 x 10⁴ splenic cells. Moreover, with age, the number of splenic colony-forming cells rapidly diminished and was significantly reduced after 6 months. Similar data were obtained when B lymphocyte clones were compared by using bone marrow and lymph node. Further, the number of B lymphocyte clones of 17-day-old NZB fetal liver was significantly higher than in control mice. Finally, of particular interest, the number of B lymphocyte clones in NZB Dh/+ mice was similar to that +/+ mice and the number of B lymphocyte clones in NZB nude mice was similar to that in nude/+ littermates, suggesting that this B cell defect is thymus independent and unrelated to antigen-nonspecific suppressor function.