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FcγR receptors activate MAP kinase and up-regulate the cyclooxygenase pathway without increasing arachidonic acid release in monocytic cells

AuthorsFernández, Nieves ; Renedo, Marta; Sánchez Crespo, Mariano
Issue Date2002
CitationEuropean Journal of Immunology 32(2): 383-392 (2002)
AbstractTHP-1 monocytic cells were stimulated with lgG-ovalbumin equivalence immune complexes (IC) and mAb reacting with both FcγRI and FcγRIIA. All of these stimuli were capable of activating the cells; however, different patterns of response were observed as regards activation of the p42-MAP/ERK kinase, triggering of the NF-κB/Rel system, production of chemotactic cytokines, and induction of the expression of cyclooxygenase-2 (COX-2). Activation of p42-MAP/ERK kinase was a constant finding, which occurred regardless of the type of stimulus applied, for instance, homotypic stimulation of a single type of receptor by cross-linking with specific mAb or heterotypic stimulation with both types of antibodies and IC. However, the activation of the MAP/ERK kinase cascade was not connected to the triggering of cytosolic phospholipase A2 (cPLA2) and arachidonic acid (AA) release. The heterotypic stimulation of FcγR induced the expression of COX-2 in a time and dose-dependent manner and activated the NF-κB system as judged from the degradation of IκB-α protein. In summary, the present data indicate that activation of the p42-MAP/ERK pathway occurs after cross-linking FcγRI and FcγRIIA receptors in monocytic cells; however, this is not coupled to the cPLA2 route, which leads to the release of AA. Noteworthy, heterotypic activation involving combined cross-linking of both FcγRI and FcγRIIA has a robust effect on the oxidative metabolism of AA by a mechanism involving κB-dependent trans-activation of COX-2.
Identifiersdoi: 10.1002/1521-4141(200202)32:2<383::AID-IMMU383>3.0.CO;2-9
issn: 0014-2980
e-issn: 1521-4141
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