
thumb|right|Staphylococcal Enterotoxin B|SEB, a typical bacterial superantigen (PDB:3SEB). The β-grasp domain is shown in red, the β-barrel in green, the "[[disulfide loop" in yellow.]] thumb|right|SEC3 (yellow) complexed with an MHC class II molecule (green & cyan). The SAgs binds adjacent to the antigen presentation cleft (purple) in the MHC-II. thumb|Schematic representation of MHC class II. thumb|The T-cell receptor complex with TCR-α and TCR-β chains, CD3 and ζ-chain accessory molecules.
thumb|right|Staphylococcal Enterotoxin B|SEB, a typical bacterial superantigen (PDB:3SEB). The β-grasp domain is shown in red, the β-barrel in green, the "[[disulfide loop" in yellow.]] thumb|right|SEC3 (yellow) complexed with an MHC class II molecule (green & cyan). The SAgs binds adjacent to the antigen presentation cleft (purple) in the MHC-II. thumb|Schematic representation of MHC class II. thumb|The T-cell receptor complex with TCR-α and TCR-β chains, CD3 and ζ-chain accessory molecules.
Superantigens (SAgs) are a class of antigens that result in excessive activation of the immune system. Specifically they cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. Superantigens act by binding to the MHC proteins on antigen-presenting cells (APCs) and to the TCRs on their adjacent helper T-cells, bringing the signaling molecules together, and thus leading to the activation of the T-cells, regardless of the peptide displayed on the MHC molecule. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system. Compared to a normal antigen-induced T-cell response where 0.0001–0.001% of the body's T-cells are activated, these SAgs are capable of activating up to 20% of the body's T-cells. Furthermore, Anti-CD3 and Anti-CD28 antibodies (CD28-SuperMAB) have also shown to be highly potent superantigens (and can activate up to 100% of T cells).
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