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EN
Immunoglobulin E plays a central role in the pathogenesis of allergic diseases. Therefore an understending of mechanisms which regulate production of IgE is very important. Recent studies have demonstrated that the induction of IgE synthesis in B cells requires two signals. The first one, IgE isotype-specific, is delivered by interleukins 4 or 13 and results in e germ line transcription. The second B-cell-activating factor is responsible for switch recombination and expression of mature eRNA transcripts. This signal is delivered by lymphocytes T, but these cells can be replaced by Epstein-Barr virus infection, protein gp39 (CD40L), monoclonal antibodies to CD40 and CD58, membrane-TNF-a, as well as corticosteroids. Besides this a variety of factors can modulate the IgE synthesis. Interleukin-2, -5, -6, -9, -10, MIPI-a, RANTES and sCD23 enhance the prodution of IgE whereas PAF, PGE2, IL-8, -12 and 18, IFN-a and g, TGF-b, sIL-4R, IL-1Ra, and probably sIL-1R inhibit it. In this article, we review current knowledge about the mechanisms underlying the synthesis of IgE in humans, including molecular events and clinical attempts at redution of the total IgE level in patients with allergic diseases.
EN
Mast cells are important effector cells in allergic inflammatory reactions. The aggregation of the high-affinity IgE receptor (Fc epsilon RI) on the surface of mast cells initiates a complex cascade of signaling events that ultimately leads to the release of various mediators involved in allergic inflammation and anaphylactic reactions. The release of these mediators is tightly controlled by signaling pathways that are propagated through the cell by specific phosphorylation and dephosphorylation events. These events are controlled by protein kinases and protein phosphatases which either positively or negatively regulate the propagation of the signal through the cell. This review summarizes the role of both positive and negative regulators of Fc?RI-induced mast cell activation.
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