Suppression of IgE synthesis in mouse plasma cells and B cells by rat IgE-suppressive factor.

Rat IgE-binding factors were assessed for the ability to regulate the IgE response of mouse spleen cells. A rat-mouse T cell hybridoma, 23B6, produced two species, i.e., 15,000 (15K) daltons and 30K daltons, of rat IgE-binding factors upon incubation with rat IgE. The 15K IgE-binding factor selectively suppressed the in vitro IgE response of DNP-KLH-primed BALB/c spleen cells to homologous antigen without affecting the IgG1 response, whereas the 30K IgE-binding factor failed to affect both the IgE and IgG1 responses. Incubation of IgE-producing hybridoma cells with the 15K IgE-binding factor resulted in a parallel decrease in the proportion of IgE-secreting cells, cytoplasmic IgE-containing cells, and sIgE+ cells. The same IgE-binding factor suppressed IgE formation by mouse plasma cells in DNP-KLH-primed or KLH-primed BDF1 mice without affecting the IgG1-forming cells. In contrast, the 30K IgE-binding factor failed to affect the formation of IgE by the hybridoma and the plasma cells. It was also found that incubation of the splenic lymphocytes with the 15K IgE-binding factor resulted in a decrease in sIgE+ B cells; the 30K IgE-binding factor failed to do so. The results indicate that the binding of the 15K IgE-binding factor to plasma cells and to sIgE+ B cells results in suppression of IgE synthesis in these cells.