title: Role of streptococcal IgG Fc receptor in tissue deposition of IgG in rabbits immunized with Streptococcus pyogenes.
abstract: Induction of anti-IgG during hyperimmunization of rabbit with Streptococcus pyogenes (group A streptococci; GAS) was previously shown to require the presence of IgG Fc receptors (FcR) in the vaccine strain. In the present work, we examined whether streptococcal FcR activity might also be of importance for heart and kidney deposition of IgG, known to occur in poststreptococcal sequelae as well as during experimental immunization of animals. Each of three IgG-binding (GAS types M1, M12 and M22) and two non-binding (GAS type T27 and S. agalactiae (GBS) type Ia) streptococcal strains were used for intravenous immunization of rabbits during two periods of eight and six weeks, respectively, separated by an interval of one month. Before use, vaccine strains were treated with KSCN and carefully washed in order to remove any surface-bound immunoglobulins. No deaths occurred among injected rabbits. No tissue deposition was elicited by the GAS type T27 or the GBS strain. In contrast, the strains of types M1, M12 and M22 all induced deposits of IgG in kidney and heart tissue, beginning during the first immunization period. In two tested animals, receiving GAS of types M1 or M22, circulating immune complexes containing anti-IgG antibodies were also detected. Finally, serum autoantibodies reacting with preparations of heart and kidney, but not lung or liver, were demonstrated in each of six animals receiving M1 or M22, reaching maximum levels during reimmunization; such antibodies were not evoked by the two strains not binding IgG. Our results suggest that, in GAS with capacity for non-immune binding of IgG, triggering of anti-IgG acted to enhance tissue deposition of IgG or immune complexes in immunized rabbits. Furthermore tissue-specific antibodies were elicited only by the IgG-binding strains and occurred comparatively late during immunization, suggesting that those antibodies might have been triggered due to the exposition of hidden kidney and heart determinants.
authors.affiliation: Institute of Experimental Medicine, Academy of the Medical Sciences, St. Petersburg, Russia.
authors.forename: L A
authors.initials: LA
authors.lastname: Burova
authors.forename: I V
authors.initials: IV
authors.lastname: Koroleva
authors.forename: R P
authors.initials: RP
authors.lastname: Ogurtzov
authors.forename: S V
authors.initials: SV
authors.lastname: Murashov
authors.forename: M L
authors.initials: ML
authors.lastname: Svensson
authors.forename: C
authors.initials: C
authors.lastname: Schalén
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis / Q000276:immunology; D000936:Antigen-Antibody Complex / Q000032:analysis; D005455:Fluorescent Antibody Technique; D007114:Immunization; D007074:Immunoglobulin G / Q000378:metabolism*; D007668:Kidney / Q000737:chemistry / Q000276:immunology / Q000648:ultrastructure; D009206:Myocardium / Q000737:chemistry / Q000276:immunology / Q000648:ultrastructure; D011817:Rabbits; D011961:Receptors, Fc / Q000032:analysis / Q000378:metabolism / Q000502:physiology*; D013292:Streptococcus agalactiae / Q000648:ultrastructure*; D013297:Streptococcus pyogenes / Q000276:immunology* / Q000648:ultrastructure; D014018:Tissue Distribution
chemical_list: D000907:Antibodies, Bacterial; D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D011961:Receptors, Fc