In both<unk>  (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen<unk> . The<unk>  in S. aureus infections is<unk> <unk> -1, or<unk> T-1. The<unk> T-1 is secreted as a single polypeptide chain. The gene encoding<unk> <unk>  is carried by a mobile genetic element of S. aureus in the SaPI family of pathogenicity islands. The<unk>  causes the non-specific binding of MHC II, on professional antigen presenting cells, with T-cell receptors, on T cells. In typical T-cell recognition, an antigen is taken up by an antigen-presenting cell, processed, expressed on the cell surface in complex with class II major histocompatibility complex (MHC) in a groove formed by the alpha and beta chains of class II MHC, and recognized by an antigen-specific T-cell receptor. This results in polyclonal T-cell activation. Superantigens do not require processing by antigen-presenting cells but instead, interact directly with the invariant region of the class II MHC molecule. In patients with<unk> , up to 20% of the body's T-cells can be activated at one time. This polyclonal T-cell population causes a cytokine storm, followed by a multisystem disease.
Toxic shock syndrome
Scarlet fever
Gulf War syndrome
Stevens–Johnson syndrome
DAVID syndrome
Septic shock
Relapsing fever
Kawasaki disease