FcR epsilon+ lymphocytes and regulation of the IgE antibody system. I. A new class of molecules, termed IgE-induced regulants (EIR), which modulate FcR epsilon expression by lymphocytes.

Exposure of unfractionated murine lymphoid cells to suitable amounts of IgE in vitro results in the de novo expression of Fc receptors for IgE (FcR epsilon) by both T and B lymphocytes. Monoclonal IgE, in the monomeric state, directly induces FcR epsilon expression by B cell-enriched but not T cell-enriched lymphoid cells. In contrast, the same monoclonal IgE in the aggregated state can directly induce FcR epsilon expression by either lymphocyte class independently. The fact that monomeric IgE induces almost equal proportions of FcR epsilon+ B and T cells unfractionated cell cultures, but can directly induce only FcR epsilon+ B cells when lymphocyte subpopulations are independently exposed to IgE, suggested the involvement of either soluble mediators or cognate interactions in this FcR epsilon expression process. Indeed, the studies presented demonstrate that IgE-stimulated lymphoid cells produce soluble mediators, termed IgE-induced regulants (EIR), which can induce FcR epsilon expression in cultures of fresh lymphoid cells. EIR-stimulated FcR epsilon expression is independent of IgE in either its native or processed state, and is largely by T cells of the Lyt-2+ subset. Thus, total depletion of T cells or more selective elimination of the Lyt-2+ subset prevented the development of FcR epsilon+ cells in cultures exposed to EIR but not in those exposed to monomeric IgE. Conversely, depletion of B cells had the opposite effect in that the remaining T cells retained the ability to express FcR epsilon in response to EIR but were unresponsive to monomeric IgE. Because of its selective activity in inducing FcR epsilon expression by T lymphocytes, EIR from unfractionated lymphoid cell cultures has been designated EIRT. This selectivity of EIRT inductive properties for T lymphocytes was additionally confirmed by analyses of the FcR epsilon+ lymphoid cells subsequent to induction with IgE or EIRT. Thus, unlike monomeric IgE, which induces FcR epsilon+ cells equally distributed among T and B lymphocytes, EIRT induces FcR epsilon+ cells in only the T cell class. These findings indicate that production of the EIRT and subsequent expression of FcR epsilon by Lyt-2+ T cells depends upon the initial interaction of IgE with B cells. Finally, an interesting paradox observed was that although IgE-induced FcR epsilon expression by B cells is unaffected by total T cell depletion, selective blocking of just Lyt-1+ T cells significantly diminishes this FcR epsilon induction process.(ABSTRACT TRUNCATED AT 400 WORDS)