1. [Antibodies to the rhamnose determinants of the polysaccharide of streptococci group A in the sera of rheumatism patients and donors].
- Author
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Borodiiuk Na, Bazanova EA, Liampert IM, Tsvetkov IuE, Bukharov AV, Bakinovskiĭ LV, Nekrasov AV, Puchkova NG, and Efimtseva EV
- Subjects
- Acute Disease, Adolescent, Adult, Humans, Immunoenzyme Techniques, Middle Aged, Recurrence, Rheumatic Heart Disease immunology, Antibodies, Bacterial blood, Blood Donors, Epitopes immunology, Polysaccharides, Bacterial immunology, Rhamnose immunology, Rheumatic Diseases immunology, Streptococcus pyogenes immunology
- Abstract
In the sera of patients with recurrent rheumocarditis, and especially in cases of primary rheumatism, the level of antibodies to group A streptococcal polysaccharide (A-PS) has been found, according to the results of the enzyme immunoassay, to be considerably higher than in the sera of healthy donors. The level of antibodies to rhamnose determinants (RD) of A-PS has been determined by the inhibition of the immunoenzyme reaction with A-PS under the influence of a variant of group A streptococcus and rhamnose disaccharides with the bonds alpha 1-2 and alpha 1-3. In patients with recurrent rheumocarditis the level of antibodies to A-PS has been shown to be considerably higher than in healthy donors having these antibodies. In acute primary rheumatism a high level of antibodies to A-PS has been detected only in a few cases, and at the same time the prevalence of antibodies to the specific RD of A-PS, bound with beta-N-acetylglucosamine, is observed. In the sera of patients with recurrent rheumocarditis and donors having a high content of antibodies to the rhamnose site of A-PS antibodies, seemingly active against at least two RD, have been detected. In acute primary rheumatism an insignificant amount of antibodies to the rhamnose site of A-PS may probably cause the autoimmune process accompanying rheumatism. This suggestion is substantiated by the previously established capacity of these antibodies for inducing the suppression of cytotoxic cell reactions to microbial antigens.
- Published
- 1991