Mechanisms involved in the binding of IgG immune complexes to sections of inflamed gingiva

Abstract

The binding of paniculate (sensitized sheep erythrocytes = EA) and soluble (horse radish peroxidase (HRP)-anti-HRP) IgG immune complexes to cryostat sections of inflamed human gingiva was studied. EA bound preferentially to inflammatory cell infiltrates in all biopsy specimens, and HRP-anti-HRP complexes were found to bind to the surface of mononuclear cells. Binding of EA was abolished by treatment of cryostat sections with 1 mM periodic acid (30 min) or 4% formaldehyde (10 min). Binding was also abolished by exposure of sections to cold ethanol for 5 min. No binding of fluorescein labelled, heat aggregated human IgG to sections of washed and ethanol-fixed biopsies of inflamed human gingiva was observed. Results of inhibition experiments with rabbit and human native or heat aggregated IgG, rabbit and human IgG Fc and IgG F(ab)2fragments, human IgGl and IgG2, mildly reduced and alkylated human IgG and with rabbit anti-human Clq, indicated that the binding is not due to activated Cl or to the presence of rheumatoid factors. Our flndings are consistent with the concept that the binding is due to the presence of IgG Fc receptors (IgGFcR) on mononuclear cells. Ethanol fixation of specimens compromises any conclusions regarding igGFcR activity in the tissues.

In situ demonstration of Fcγ‐receptors in human chronic marginal and periodontitis

“…In our previous work (3,5) in whieh only funetional assays were used, we were able to localize FeyR mainly to certain mononuclear cells in the infiltrated eonneetive tissue. By prolonging the ineubation time of the soluble immune eomplexes and by means of a monoelonal antibody, we have been able to loealize FcyR also to fibrous elements, endothelial eells, lyr-nphoeytes within epithelial elements and keratinoeytes.…”

“…Psoriatic skin lesions have an enhanced expression of FcyR on endothelial cells, more strongly in clinically active than in inactive lesions (20). We have previously reported the bindng of soluble immune complexes to cryostat sections of chronic marginal periodontitis (5). In those studies we were not able to give reliable documentation of endothelial FcyR.…”

“…Receptors for the Fc portion of the IgG molecule (FcyR) have been demonstrated in eryostat sections of both marginal and apieal periodontitis by using sheep erythrocytes (E) sensitized with IgG antibodies (A) to E to form particulate immune complexes (EA) (1)(2)(3)(4)(5)(6). In both types of lesions, EA bound strongly to the inflammatory tissue, and the adherenee was strongest in the most intensely infiltrated areas (3,5).…”

Variation in the composition of gingival inflammatory cell infiltrates

“…Reinhardt et al (1988a, b), for their immunohistochemical studies, distinguished between "active" and "stable" sites on the basis of repeated clinical tneasurements. In our investigations (Kristoffersen et al 1985, Johannessen et al 1986), we have not attempted to group the lesions according to clinical disease activity. Errors of the clinical measurements involved are considerable and reportedly account for a high % of false positive rates in detection of episodes of disease activity (Rails & Cohen 1986, Cohen & Rails 1988).…”