Comparison of the clonal diversity of the B cell repertoires in adult mice that differ in the expression of cell surface IgD.

To determine whether the expression of surface IgD (sIgD) influences the extent of the expressed B cell repertoire, the clonal diversity of the B cell population in mice treated chronically with anti-IgD (delta) antibodies has been compared with the B cell repertoire observed in control animals, using the splenic focus limiting dilution B cell assay. The results show that the phosphorylcholine (PC)-specific B cell precursor frequency in anti-delta antibody-treated mice is increased when compared with that of control mice. Isotype and idiotype (T15) analyses of PC clonal products from anti-delta antibody-treated and control mice revealed no distributional differences. Analyses of the 2,4-dinitrophenyl (DNP)- and fluoresein isothiocyanate-specific B cell repertoires confirmed that the equal or increased precursor frequencies observed in anti-delta antibody-treated mice are not specific for the PC antigen. The increased precursor frequency of B cells from anti-delta antibody-treated mice was not the result of increased homing of B cells from anti-delta antibody-treated mice to recipient spleens, since B cells from control mice homed twice as well to recipient spleens as did B cells from anti-delta antibody-treated mice. Other studies demonstrated that (a) on average, antibody-secreting clones were generated more slowly when B cells from anti-delta antibody-treated mice were used as a source of precursors than B cells of control mice and (b) both sIg- spleen cells and sIg+ spleen cells from anti-delta antibody-treated mice generated a higher frequency of specific antibody-secreting clones than did the corresponding populations from control mice. These observations suggest that a population of sIgM+sIgD- B cells exists that resembles sIgD+ B cells rather than neonatal or xid B cells in its ability to generate responses to PC and suggests that the sIgM+sIgD- B cells from anti-delta antibody-treated mice are more responsive than are sIgM+IgD+ B cells, regardless of antigenic specificity, to the stimuli provided in the splenic focus system. Finally, this study suggests that the expression of sIgD does not influence the extent of the expressed B cell repertoire.