Published in Volume 68, Issue 3 (September 1981)
J Clin Invest. 1981;68(3):665–671. doi:10.1172/JCI110301.
Copyright © 1981, The American Society for Clinical Investigation.

Articles

Cellular Immune Responses to Extracellular Streptococcal Products in Rheumatic Heart Disease

Ernest D. GrayLewis W. WannamakerElia M. AyoubAziz El KholyZahira H. Abdin

^{Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota 55455}^{Department of Biochemistry, Medical School, University of Minnesota, Minneapolis, Minnesota 55455}^{Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota 55455}^{Department of Microbiology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455}^{Department of Pediatrics, University of Florida College of Medicine, Gainesville, Florida 32610}^{Biomedical Research Center for Infectious Diseases, Cairo, Egypt}^{Rheumatic Heart Center, Cairo University, Cairo, Egypt}

Published September 1981

The lymphocyte transformation responses to purified preparations of two extracellular products of group A streptococci (blastogen A and nuclease B), to phytohemagglutinin, and to Candida albicans antigen were measured in tonsillar and peripheral blood lymphocytes from patients with rheumatic heart disease (RHD) and suitably matched nonrheumatic (control) subjects.

The mean phytohemagglutinin dose responses of tonsillar and peripheral lymphocytes from RHD patients were essentially indistinguishable from those of controls. In contrast, the responses of tonsillar and peripheral blood lymphocytes to the two extracellular products of group A streptococci were significantly lower in RHD patients than in nonrheumatic control subjects. Candida antigen produced very little stimulation of lymphocytes in any of the subjects.

The geometric means of antibody levels against streptolysin O, nuclease B, and nicotinamide adenine dinucleotidase showed no consistent differences between the control group and the group of RHD subjects. Group A streptococci were isolated from the tonsils of ∼25% of both groups of subjects.

The RHD patients clearly had a depressed cellular immune response to the two purified streptococcal extracellular antigens. The equal frequency in recovery of group A streptococci from tonsils and the absence of consistent difference in titers of humoral antibodies to streptococcal extracellular antigens, particularly nuclease B, suggest that this differential response is not due to a lower level of stimulation by repeated exposure to group A streptococcal products.