The excessive activation of an unusual high proportion of T lymphocytes and APCs in vivo and in vitro upon binding the SAg molecules triggers massive production of a wide array of inflammatory and other Th1/Th2 and APC-derived cytokines, by the stimulated cells. This process takes place through a complex of upregulated and downregulated immunological networks, activation signals, and the cooperation of adhesion molecules on target cells leading to a cascade of events including further release (besides cytokines and chemokines) of other pharmacologically active products, particularly those of
the arachidonic acid/lipid pathways.[ ,,,] This SAgmediated hyperstimulation of the immune system of the host can overwhelm the host regulatory network and thereby assist pathogen evasion of the adaptive immune response. Moreover, the excessive and aberrant activation of T cells causes damage to tissues and organs and cell apoptosis which may result in disease and even death.[13,22] Superantigen activity, particularly SPE A, has been found in acute-phase serum samples from strepto-coccal disease patients.
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