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Signal Transduction Pathways Regulating Arachidonic Acid Metabolite Generation Following FcεRI Aggregation

  • Chapter
Book cover IgE Receptor (FcεRI) Function in Mast Cells and Basophils

Part of the book series: Molecular Biology Intelligence Unit ((MBIU))

Abstract

Aggregation of high affinity IgE receptors (FcεRI) on the surface of ast cells and basophils results in the initiation of specific signal transduction events that lead to degranulation, cytokine gene expression and the de novo synthesis and release of phospholipid-derived pro-in- flammatory mediators. The phospholipid-derived category of inflamma- tory mediators includes cyclooxygenase-derived products such as prostag- landin (PG) D2, 6-keto-PGF1α, PGE2 and thromboxane B2; and 5-lipoxygenase-derived products such as leukotriene (LT) C4, LTB4 and LTE4.1−17 Two major steps are required for the generation of these inflammatory mediators from phospholipids: (a) the liberation of substrate, i.e., arachidonic acid from phospholipids, and (b) the generation of the active metabolites from arachidonic acid (Fig. 10.1). Although it is likely that the early signal transduction events in the FcεRI-mediated production of these molecules are similar to those leading to degranulation and perhaps cytokine gene expression, there is emerging evidence indicating that there is also divergency in these pathways.

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Gilfillan, A.M. (1997). Signal Transduction Pathways Regulating Arachidonic Acid Metabolite Generation Following FcεRI Aggregation. In: IgE Receptor (FcεRI) Function in Mast Cells and Basophils. Molecular Biology Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-22022-1_10

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