Regulation of human IgE synthesis by soluble factors. Papain treatment of a FcE receptor-positive B-cell line (RPMI-1788) releases regulatory factors for IgE synthesis.

Abstract

A novel mechanism for the release of helper and suppressor factors for human IgE synthesis is described. When FcE receptor-positive RPMI-1788 cells are treated with papain, a helper factor(s) for human IgE synthesis is released. At the same time a significant decrease in the number of cell surface FcE receptors is observed. The immunoglobulin synthesis-enhancing activity is IgE isotype-specific inasmuch as the same supernatant suppresses the synthesis of human IgA myeloma cells. When the FcE receptor-positive RPMI-1788 cells are treated with tunicamycin and then with papain, a suppressor factor(s) for human IgE synthesis is released. The mechanism by which these factors affect human myeloma IgE synthesis is unclear at present. Our results indicate that enhanced IgE synthesis is not due to increased numbers of secreting cells nor to an increased release of presynthesized IgE. In summary, papain treatment of FcE receptor-positive, but not FcE receptor-negative cells, generates a factor that regulates IgE synthesis. These results also provide evidence for the close relationship between the IgE regulatory factors and the low affinity receptors for IgE present on lymphocytes.