IgE-binding factors and regulation of the IgE antibody response.

In rodents, IgE-bF are derived from a subset of T cells that bear Fc epsilon R or Fc gamma R, or both, and selectively enhance or suppress the IgE response. IgE-PF and IgE-SF may share a common structural gene, therefore a common polypeptide chain, and their biologic activities are decided by post-translational glycosylation process. Under physiological conditions, this process is controlled by two lymphokines, i.e. GEF and GIF. The same principle probably applies to human T cell-derived IgE-bF. In both rodent and human lymphocytes, Fc epsilon RII on B cells are degraded, and their fragments are released from the cells. The fragments of Fc epsilon RII on human B cells represent the carboxy terminal half of the receptor molecules and have affinity for IgE. In contrast, the fragment of Fc epsilon R in mouse B cells does not have an affinity for IgE. Thus, "IgE-bF" are derived from both T cells and B cells in humans, but only from T cells in rodents. The formation of T cell-derived IgE-bF was induced by interferons, while biosynthesis of Fc epsilon R in B cells and the formation of their fragments were enhanced by IL-4. IgE-bF are also formed by a subset of antigen-primed T cells upon cognate interaction with antigen-pulsed syngeneic macrophages. These antigen-primed T cells constitutively secrete either GEF or GIF, having no affinity for homologous antigen. Upon antigenic stimulation, however, GEF and GIF formed by the cells had affinity for the antigen. The antigen-specific GEF enhanced the antibody response, and antigen-specific GIF suppressed the antibody response, both in carrier specific manner. The possible relationship between antigen-specific GEF and antigen-specific TaF, and that between antigen-specific GIF and antigen-specific TsF both require further studies. Nonspecific GIF not only switches T cells from the formation of IgE-PF to the formation of IgE-SF, it also facilitates the generation of antigen-specific suppressor T cells which produce antigen-specific GIF upon antigenic stimulation. Propagation of antigen-primed T cells in the presence of GIF also facilitate the generation of antigen-specific suppressor T cells in vitro. If the same procedures would be effective for human T cells of allergic patients, it would be possible to generate antigen-specific suppressor T cells from their T cell population in vitro and to establish T cell hybridomas that produce allergen-specific GIF(TsF).(ABSTRACT TRUNCATED AT 400 WORDS)