Regulation of the human IgE antibody response.

The frequent association of elevated serum IgE in patients with T cell immunodeficiencies suggest a role for T cells in the regulation of the human IgE antibody response. Unlike the situation with other isotypes the polyclonal B cells activators, pokeweed mitogen and Epstein Barr virus, do not routinely induce IgE synthesis in normal B cells. However, B cells from normal donors will synthesize immunoglobulins of all isotypes (including IgE) when cultured with T cell clones that recognize determinants expressed on the B cells (cognate stimulation). T cells with Fc receptors for IgE can be isolated from patients with hyper IgE syndrome and maintained as long term continuous T cell lines. These cells secrete IgE binding factors which enhance IgE synthesis but not IgG synthesis by preactivated IgE bearing B cells from allergic subjects but not resting B cells from normal donors. IgE binding factors isolated from sera of normal donors selectively suppress IgE synthesis. In contrast, IgE binding factors isolated from sera of patients with hyper IgE syndrome contain IgE potentiating activity as well as IgE suppressor activity. These results suggest that IgE synthesis in man is activated by T cells and isotype specific secretion of this immunoglobulin is modulated by IgE binding factors.