Cellular reactivity studies to streptococcal antigens. Migration inhibition studies in patients with streptococcal infections and rheumatic fever.
The question of whether hypersensitivity to streptococcal antigens plays a role in the pathogenesis of the nonsuppurative sequelae of streptococcal infections remains at present unclear. As a first step in the approach to this question, the degree of cellular reactivity of peripheral blood leucocytes to streptococcal antigens was investigated in a number of rheumatic fever patients, patients with uncomplicated streptococcal infections, as well as normal healthy subjects. Using the in vitro technique for the inhibition of capillary migration of peripheral blood leucocytes as an index of the degree of sensitivity to streptococcal antigens, the results indicate that patients with acute rheumatic fever exhibit an exaggerated cellular reactivity to these antigens and in particular to streptococcal cell membrane antigens. This abnormal response to streptococcal membrane antigens appears to persist in rheumatic subjects for at least 5 yr after the initial attack of rheumatic fever. Only Group A streptococcal membrane antigens elicited this unusual response in rheumatic subjects, since the cellular reactivity to Group C and D streptococcal membranes was the same in all groups. Patients with evidence of valvular disease exhibited the same degree of cellular reactivity to these antigens as did patients without clinical evidence of rheumatic heart disease. The nature of the antigens responsible for the observed cellular response remains unknown. Enzymatic treatment of streptococcal cell walls and membranes designed to remove type-specific M proteins did not alter the observed cellular reactivity to the streptococcal antigens. The finding that an abnormal cellular response to certain streptococcal antigens is present only in rheumatic patients suggests that cell-mediated factors may play an important role in the disease process.
D000818:Animals; D000906:Antibodies / Q000032:analysis; D000942:Antigens, Bacterial; D000989:Antistreptolysin / Q000032:analysis; D002462:Cell Membrane / Q000201:enzymology / Q000276:immunology; D002464:Cell Migration Inhibition; D002473:Cell Wall / Q000276:immunology; D003470:Culture Media; D046508:Culture Techniques; D006349:Heart Valve Diseases / Q000276:immunology; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000150:complications / Q000276:immunology; D007111:Immunity, Cellular; D007962:Leukocytes / Q000276:immunology*; D009206:Myocardium / Q000276:immunology; D011817:Rabbits; D012213:Rheumatic Fever / Q000097:blood / Q000201:enzymology / Q000209:etiology / Q000276:immunology*; D013290:Streptococcal Infections / Q000097:blood / Q000201:enzymology / Q000209:etiology / Q000276:immunology*; D013291:Streptococcus / Q000276:immunology*; D013297:Streptococcus pyogenes / Q000276:immunology; D014357:Trypsin
D000906:Antibodies; D000942:Antigens, Bacterial; D003470:Culture Media; D000989:Antistreptolysin; D014357:Trypsin