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J. Biol. Chem., Vol. 278, Issue 52, 52179-52187, December 26, 2003

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Release of Arachidonic Acid by Stimulation of Opsonic Receptors in Human Monocytes

THE FcR AND THE COMPLEMENT RECEPTOR 3 PATHWAYS^*

Nieves Fernández, Marta Renedo¶, Sara Alonso¶, and Mariano Sánchez Crespo¶||

From the Unidad de Investigación Hospital Clínico Universitario, 47005-Valladolid, Spain and the ^¶Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, 47005-Valladolid, Spain

The role of the opsonic receptors FcR and CR3 on the release of arachidonic acid (AA) by human monocytes was studied using IgG-ovalbumin (OVA) equivalence immune complexes (IC), anti-OVA IgG bound to OVA-coupled latex beads, and C3bi-bound IC. Release of AA was produced by IC and latex-OVA beads bound to IgG, whereas binding of C3bi to IC inhibited the ability of IC to release AA. In contrast, coating of zymosan particles with C3bi enhanced AA release as compared with that produced by non-coated particles. Masking of C3bi on C3bi-bound IC by incubation with anti-C3 IgG resulted in the recovery of their ability to release AA, thereby suggesting that binding of C3b by IC reduces their flogogenic effects, whereas opsonization of microbial walls by complement may enhance their proinflammatory potential. The binding/uptake of opsonized zymosan particles was inhibited by anti-CR3 Ab and C3bi-bound IC, but not by -glucan, mannan, and anti-Toll-like receptor 2 Ab. These findings show that cooperative engagement of CR3 on both the lectin-like site involved in -glucan binding and the I-domain involved in C3bi binding, as it can be observed in the innate immune response, produces AA release, whereas the unique interaction of C3bi-bound IC with the I-domain of CR3, as it may occur in the adaptive immune response, diverts the IC lattice from a productive interaction with FcR linked to AA release.

Received for publication, October 3, 2003

^* This study was supported by Grant SAF2001-0506 from Plan Nacional de Salud y Farmacia. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both authors contributed equally to this work.

^|| To whom correspondence should be addressed: Instituto de Biología y Genética Molecular, Facultad de Medicina, 47005-Valladolid, Spain. Tel.: 34-983-423273; Fax: 34-983-423588; E-mail: mscres{at}ibgm.uva.es.

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