title: Immune complex-FcgammaR interaction modulates monocyte/macrophage molecules involved in inflammation and immune response.
abstract: The interaction between receptors for the Fc portion of IgG (FcgammaRs) from monocytes/macrophages and immune complexes (IC) triggers regulatory and effector functions. Recently, we have demonstrated that IC exert a drastic inhibition of basal and IFN-gamma-induced expression of MHC class II on human monocytes. Taking into account that the regulation of MHC class II molecules is a crucial event in the immune response, in this report we extend our previous studies analysing the effect of STAT-1 phosphorylation in the down-regulatory process, the fate of the intracellular pool of MHC class II molecules and the effect of complement on MHC class II down-regulation induced by IC. We also studied the effect of IC on the expression of MHC class II (I-A(d)) in macrophages using a mouse model of chronic inflammation. We demonstrate that IC induce a depletion not only on surface expressed but also on intracellular MHC class II content and that IC-induced down-regulation of MHC class II is not mediated by the inhibition of STAT-1 phosphorylation. On the other hand, the effect of IC is not specific for the down-regulation of MHC class II, for it could be restricted to other molecules involved in inflammatory processes. Our experiments also show that the activation of the complement system could be a crucial step on the regulation of the effect of IC on MHC class II expression. In agreement with our in vitro experiments using human monocytes, IC treatment reduces the expression of MHC class II in a mouse model of chronic inflammation.
authors.affiliation: CONICET, División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina.
authors.forename: P
authors.initials: P
authors.lastname: Barrionuevo
authors.forename: M
authors.initials: M
authors.lastname: Beigier-Bompadre
authors.forename: G C
authors.initials: GC
authors.lastname: Fernandez
authors.forename: S
authors.initials: S
authors.lastname: Gomez
authors.forename: M F
authors.initials: MF
authors.lastname: Alves-Rosa
authors.forename: M S
authors.initials: MS
authors.lastname: Palermo
authors.forename: M A
authors.initials: MA
authors.lastname: Isturiz
mesh_terms: D000818:Animals; D000936:Antigen-Antibody Complex / Q000378:metabolism*; D002478:Cells, Cultured; D002908:Chronic Disease; D003165:Complement System Proteins / Q000276:immunology; D004268:DNA-Binding Proteins / Q000378:metabolism; D015536:Down-Regulation / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000276:immunology*; D010766:Phosphorylation; D017452:Receptors, IgG / Q000378:metabolism*; D050794:STAT1 Transcription Factor; D015534:Trans-Activators / Q000378:metabolism
chemical_list: D000936:Antigen-Antibody Complex; D004268:DNA-Binding Proteins; D000949:Histocompatibility Antigens Class II; D017452:Receptors, IgG; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; C494080:Stat1 protein, mouse; D015534:Trans-Activators; D003165:Complement System Proteins