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题目:: FcR epsilon+ lymphocytes and regulation of the IgE antibody system. II. FcR epsilon+ B lymphocytes initiate a cascade of cellular and molecular interactions that control FcR epsilon expression and IgE production.
作者:: Marcelletti(J F),Katz(D H)
状态:: 发布时间1984-12-19 , 更新时间 2007-11-14
期刊:: J Immunol
摘要:: This study additionally explores the orderly sequence of events concerning the induction of Fc receptors for IgE (FcR epsilon) that are initiated by IgE and mediated by IgE-induced regulants (EIR). Thus, lymphoid cells exposed to monomeric IgE displayed an early phase of exclusive B cell FcR epsilon expression, followed by the progressive appearance of FcR epsilon+ T cells, ultimately resulting in equal proportions of FcR epsilon+ B cells and T cells. Parallel cultures of lymphoid cells stimulated with EIR derived from unfractionated lymphoid cells (EIRT) also manifested rapid induction of FcR epsilon+ cells, but these FcR epsilon+ cells were predominantly T cells from the outset. Data presented here demonstrate that IgE-induced FcR epsilon expression by B cells ultimately results in the production of EIRT, which then induces FcR epsilon expression by T cells. The existence of EIRT that selectively induce T cell FcR epsilon expression prompted us to search for an EIRB that is selectively active in inducing FcR epsilon+ B cells. Indeed, IgE-stimulated, T cell-depleted lymphoid cells produce an EIRB that selectively induces FcR epsilon expression by B cells. This EIRB, but not EIRT, can also be generated by IgE stimulation of Lyt-2+ cell-blocked lymphoid cells, indicating that Lyt-1+ cells are not inhibitory to EIRB production and that production of EIRT is dependent upon functionally competent Lyt-2+ cells. Similar to IgE, EIRB induces rapid FcR epsilon expression, first by B cells and then by T cells, so that by 16 hr post induction equal proportions of FcR epsilon+ B and T cells were observed. Although complete T cell depletion does not affect IgE-induced FcR epsilon expression, selective blocking of Lyt-1+ cells markedly diminishes such responses, suggesting that Lyt-2+ cells are antagonistic to the induction of FcR epsilon+ B cells. Studies involving sequential T cell subset depletion clearly demonstrated that in the absence of functionally competent Lyt-1+ cells, Lyt-2+ cells exert an inhibitory influence on IgE-induced FcR epsilon expression by B cells. Stimulation of Lyt-1+ cell-blocked cultures with EIRT, and to a lesser degree with IgE, resulted in the elaboration of an EIR (EIRI), which lacks direct FcR epsilon-inductive properties, but conversely, directly inhibits IgE-induced FcR epsilon expression in fresh B cell cultures.
语言:: eng
DOI:

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