Acute rheumatic fever
ARF occurs within 10 days to six weeks after an episode of GAS pharyngitis, although the causative infection may be subclinical. It occurs as a nonsuppurative complication of GAS pharyngitis in susceptible hosts. While the underlying mechanisms of ARF are not well understood, the key event is inappropriate activation of the immune system, leading to autoimmune attack.
Invading pathogens trigger innate immune responses, leading to inflammation. During the inflammatory response, immune cells are attracted to the site of infection and are exposed to antigenic compounds. Antigenic compound in GAS infections include the M-protein, hyaluronic acid coat and exotoxins.
the presentation of an antigen to the cells of the immune system (T-lymphocytes) is mediated by the human leucocyte antigen (HLA) system are leads to the production of antibodies and memory cells. HLA genes are subject to variation : the incidence of ARF is associated with certain types of HLA complexes. GAS antigens, in particular M-protien, associated with HLA, mimic protein complexes of host tissue and trigger cross-reactivity. The antibodies produced against GAS begin to attack host-tissue.