Pathogenesis of Rheumatic Fever



Pathogenesis of rheumatic fever. 

1. GAS pharyngitis leads to antigenic presentation of pathogenic peptides to T-cells. 

2. In immunologically susceptible individuals, the innate and adaptive (both humoral and cellular) immune responses gets activated leading to the development of cross-reactive antibodies and cross-reactive T-cells which incites immune response in the joints, heart, skin, and brain leading to different manifestations of ARE. 

3. In the heart, valve damage is initiated by endothelial activation' by cross-reactive antibodies which trigger increased expression of vascular cell adhesion molecule-I (VCAM-I). This facilitates T-cell infiltration leading to cytokine-mediated immune damage. Exposure of Type-IV collagen can lead to production of collagen-specific antibodies which can cause further damage. 

4. In the brain, autoantibodies can target dopamine receptors and lysoganglioside leading to increased release of dopamine by the neurons thereby causing rheumatic chorea 



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