Polyclonal activation of the murine immune system by an antibody to IgD. IV. In vivo activation of B lymphocytes from immune defective CBA/N mice.

Previous studies with BALB/c mice have established that the injection of a goat antibody to IgD (GaM delta) induces splenic B lymphocytes to undergo T-independent, polyclonal increases in cell surface (s) Ia expression, size, and DNA synthesis 1 day after injection, as well as T-dependent maintenance of this activation and differentiation into sIgG1+ cells and IgG1-secreting cells 6 to 7 days after injection. Because B lymphocytes from mice homozygous or hemizygous for the CBA/N X-linked immune defect fail to proliferate in vitro when cultured with soluble anti-Ig antibodies, yet can make in vivo primary antibody responses to T-dependent antigens, we studied the effects of injecting (CBA/N X DBA/2)F1 male mice (immune defective) and (CBA/N X DBA/2)F1 female mice (phenotypically normal) with 800 to 1600 micrograms of GaM delta. B cells from immune defective mice demonstrated definite but distinctly subnormal increases in B cell size, DNA synthesis, and sIa expression 1 to 5 days after GaM delta injection, but by day 7 showed increases in these parameters as well as in the percentages of splenic sIgG1+ cells and IgM-secreting cells that were similar to those exhibited by the immunologically normal mice. However, IgG1 secretion by the immune defective mice was at this time only one-fourth to one-half as great as that observed with normal mice. Our data raises the possibility that the differentiation of B cells into IgG1-secreting cells may be more dependent upon the GaM delta-induced activation steps that are defective in CBA/N mice than is the differentiation of B cells into IgM-secreting cells or into sIgG1 cells.