Immune complexes suppressed IFNã-induced up-regulation of FcãRI on human

EVANGELINA A. LABORDE; VERÓNICA I. LANDONI; M. BÁBARA REARTE; GABRIELA FERNANDEZ; MARTÍN A. ISTURIZ

Viña del Mar, Chile

Congreso; IX Congreso Latinoamericano de Inmunología; 2009

ALAI

Interferon g (IFNg) is a pleiotropic cytokine that plays a crucial role on immune response regulation and is produced during an autoimmune disease with circulating immune complexes (IC). Furthermore, IFN-g modulates FcgRI expression, the type I receptor for the Fc portion of IgG. Taking into account that IC interact with FcgRs triggering regulatory and effector functions, we evaluated the effect of IFN-g and IC on FcgRI expression on immature monocyte-derived dendritic cells (iDCs). For this purpose, iDCs were treated with IFN-g for 18h and then FcgRI expression was evaluated by flow cytometry. FcgRI up-regulation was induced by IFN-g on iDCs (15.28±2.7; 40.12±4.3; p<0.0001) moreover, a synergic effect was observed when iDCs were pretreated with IFN-g for 2h before adding dexamethasone (DEX) for 18h (83.67± 6.1; p=0,0047). On the other hand, IC abrogated IFNg induced up-regulation of FcgRI (20.82±4.3; p=0,0013). However, a partial restoration of FcgRI up-regulation was observed when IC were added in combination with DEX (30.31±4.3; p=0,0047). Neither IC nor DEX altered FcgRI expression. The results presented herein, the, suggest the existence of different mechanisms capable of modulating FcgRI expression during an inflammatory process.