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The importance of group A hemolytic streptococcal infections in the pathogenesis of rheumatic fever is widely recognized, but little is known of the mechanism by which the streptococcal infection gives rise to the disease. The concept that an antigen-antibody interaction may be involved in the origin of the pathologic processes has received increasing attention, and recent antibody studies (1, 2) provide suggestive evidence in support of this point of view. For example, studies in several laboratories dealing with a variety of streptococcal antigens have demonstrated that the mean antibody response of a group of rheumatic fever patients to these antigens is greater than that of a comparable group of patients with uncomplicated streptococcal disease (3-6). In view of these findings, it is of importance to determine whether the hyperreactivity of rheumatic subjects is limited to antigens derived from the streptococcus or is a reflection of a fundamental difference which would be demonstrable in an enhanced response to a va

the journal of clinical investigation/the journal of clinical investigation

STUDIES OF DIPHTHERIA ANTITOXIN IN RHEUMATIC FEVER SUBJECTS: ANALYSIS OF REACTIONS TO THE SCHICK TEST AND OF ANTITOXIN RESPONSES FOLLOWING HYPERIMMUNIZATION WITH DIPHTHERIA TOXOID