Final answer:
Superantigens trigger unregulated T-cell activation by binding outside the antigen-binding cleft of MHC II and interacting with TCRs, leading to a nonspecific cytokine storm and severe inflammation.
Step-by-step explanation:
The mechanism by which superantigens induce unregulated T-cell activation contrasts with the action of conventional antigens. Typical antigens are presented to T cells by Antigen-Presenting Cells (APCs) and are recognized in a highly specific manner, involving the antigen-binding cleft of Major Histocompatibility Complex (MHC) molecules. In comparison, superantigens bind outside the antigen-binding cleft of MHC II molecules and interact with the variable beta region of T-Cell Receptors (TCRs), bypassing the specificity of antigen recognition. This results in the activation of a large percentage of T cells, irrespective of their antigen specificity.
Such an activation leads to a massive release of cytokines, a harmful condition known as the cytokine storm. This can provoke severe inflammatory reactions, causing symptoms such as high fevers, low blood pressure, and potentially fatal conditions like multi-organ failure and shock. Superantigens are produced by various bacterial and viral pathogens, including those that cause toxic shock syndrome and scarlet fever. Unlike regular antigens that result in a precise immune response, the response to superantigens is excessive and can lead to serious health consequences.