Rheumatogenic streptococci and autoimmunity

The uniqueness of the group A streptococcus in initiating a cardiodestructive disease in a limited segment of the human species, regardless of race or ethnic group, makes the quest for a unique host response to a specific streptococcal antigen an intriguing and persisting challenge for clinical investigators, particularly for those investigators interested in autoimmunity. New methodology is making possible more incisive research approaches. The defined streptococcal antigens that turn out to be epitopes identical with host tissues, such as the M protein/cardiac myosin model or the hyaluronate in the capsule of mucoid rheumatogenic strains, offer the opportunity for more incisive clinical investigations. The isolation and cultivation of cardiotoxic T cell clones directed against such epitopes shared by host and parasite may eventually be possible. We may then learn more about whether autoimmunity is indeed a factor in the pathogenesis of rheumatic heart disease.