Differential capacity of various anti-Ig reagents to synergize with interleukin-4 to induce clonal expansion in resting and activated B cells.

The regulation of B cell growth responses by cross-linking of surface Ig receptors by monoclonal or polyclonal antibodies and its interaction with interleukin-4 (IL-4) has been evaluated. High-density B cells from autoimmune NZB/W mice were proliferated in the presence of low concentrations of a polyclonal goat anti-mu antibody and IL-4. Similarly, slight but significant positive responses were obtained with anti-K monoclonal antibodies and IL-4. In contrast, the same concentration of other surface Ig binding agents such as monoclonal antibodies against mu and delta immunoglobulin heavy chains did not synergize with IL-4 in order to induce clonal expansion of resting B cells. Polyclonal and monoclonal anti-Ig reagents inhibited the spontaneous cell growth of low-density B cells (in vivo activated B cells), although the negative effect was less noticeable with anti-delta monoclonal antibodies. Upon addition of IL-4 to activated B cell cultures in the presence of goat anti-mu antibody, a significant proliferative response was obtained. However, this lymphokine was unable to induce clonal expansion of B cell blasts in the presence of the various monoclonal anti-Ig antibodies employed in this study. Similar results were obtained with splenic B cells from normal animals, suggesting that the results shown in this report are not due to putative functional peculiarities of autoimmune B cells.