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dc.contributor.authorFernández, Nieves-
dc.contributor.authorRenedo, Marta-
dc.contributor.authorSánchez Crespo, Mariano-
dc.identifierdoi: 10.1002/1521-4141(200202)32:2<383::AID-IMMU383>3.0.CO;2-9-
dc.identifierissn: 0014-2980-
dc.identifiere-issn: 1521-4141-
dc.identifier.citationEuropean Journal of Immunology 32(2): 383-392 (2002)-
dc.description.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.-
dc.description.sponsorshipThis work was supported by grants from Plan Nacional de Salud y Farmacia (grant SAF98-0176), and CICYT and European Commission (grant 1FD-2325).-
dc.titleFcγR receptors activate MAP kinase and up-regulate the cyclooxygenase pathway without increasing arachidonic acid release in monocytic cells-
dc.description.versionPeer Reviewed-
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