Sera from 173 healthy adults and 55 rheumatoid patients were studied for IgG-, IgM- and IgA-rheumatoid factors (RFs) by a modification of Este's indirect immunofluorescence method. Rabbit IgG bound to smeared sheep red cells was used as antigen. With each serum tested a smear on non-sensitized cells was used as control antigen. Anti-IgG of the sera studied, binding to the antigen, was demonstrated by fluorescein-conjugated antisera, monospecific for gamma, mu and alpha chains, and not containing antibodies to sheep erythrocytes or rabbit IgG. Positive reactions were obtained with IgG as antigen, but not with the F(ab')2 fragment. The sera tested were treated with dithiothreitol before they were assayed for IgG-RF, in order to abolish false-positive reactions due to IgM-RF activity. The detection limit for IgM-RF was 1 IU per ml. IgM-RF titres of 9 occurred in 7% of healthy adults and 73% of rheumatoid patients, titres greater than or equal to 18 in 3.5% and 67% respectively. IgG-RF titres of 9 occurred in 9% of healthy adults, 21% of seronegative and 24% of seropositive rheumatoid patients. Titres of 18 occurred in 3% of healthy adults and in 14% of seronegative rheumatoid patients. Titres of greater than or equal to 18 occurred in 22% of seropositive rheumatoid patients. IgG-RF was correlated with an involvement of more than 20 joints. IgA-RF was found in 83% of seropositive, 11% of seronegative rheumatoid patients and in none of the healthy adults (serum dilution 1:9).
Anti-IgG antibodies (anti-IgG) of the IgE class were studied in sera from patients with juvenile rheumatoid arthritis (JRA), rheumatoid arthritis (RA) and patients with Felty's syndrome (FS) by use of an indirect immunofluorescence technique. Forty-two per cent of 26 patients with JRA had IgE anti-IgG in serum all in low titers. Positive reactions prevailed in patients with multiple joint involvement. Sixty-three per cent of 30 patients with RA and 80% of 20 patients with FS had IgE anti-IgG, the titers found in FS patients being significantly higher. In JRA and FS patients the IgE anti-IgG titers were correlated to the titers of anti-IgG of the IgG class, and for FS patients also with the IgM and IgA classes of anti-IgG. In six of 10 patients with RA the synovial fluid samples from both knees contained IgE anti-IgG. In four of these patients the titers of IgE anti-IgG were higher than in the corresponding serum sample, pointing to a local production. After G-200 Sephadex chromatography IgE anti-IgG were demonstrated in the void volume indicating the presence of these autoantibodies in immune complexes. IgE anti-IgG may be involved in the pathogenesis of JRA and RA by eliciting Type I and III reactions.
With an indirect immunofluorescence technique 77% of 96 patients with type I allergy and 40% of 20 patients with intrinsic bronchial asthma showed positive reactions for IgG anti-IgG antibodies in serum. They were present partly in an aggregated state not directly detectable before treatment with dithiothreitol. The aggregates could be removed by precipitation with polyethylene glycol. The IgG anti-IgG in hyposensitized patients were directed against both F(ab')2 and Fc fragments of rabbit IgG. Thirty of the type I allergic patients were examined once during hyposensitization as well. Before treatment 87% had IgG anti-IgG (titres 9-72). After greater than or equal to 13 months of treatment 100% were positive (titres 36-288). Eight patients were also examined after hyposensitization had been discontinued for at least 12 months. The titres of IgG anti-IgG had then reverted to the levels obtained before hyposensitization. Of 116 controls matched for sex and age, 7% had IgG anti-IgG antibodies. It is suggested that the production of IgG anti-IgG may be stimulated by the presence of immune complexes and that purity, amount and/or combination of allergens administered during hyposensitization may influence the production of anti-IgG antibodies. Neither IgE anti-IgG nor antinuclear antibodies seem to be of particular significance in allergic patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.