RNase Protection Assay for the Study of the Differential Effects of Therapeutic Agents in Suppressin

Staphylococcal exotoxins (SE) are among the most common etiological agents that cause toxic shock (1 ). Similar to other superantigens, SE activates T cells polyclonally by binding simultaneously to specific Vβ regions of T-cell receptors (TCR) on T cells and the major histocompatibility complex class II (MHC II) molecules on antigen-presenting cells (APCs) (2 ,3 ). Interaction of SE with TCR and MHC II results in a massive release of proinflammatory cytokines from stimulated cells (4 ,5 ). Previous studies demonstrated that the cytokines produced, tumor-necrosis factor (TNF-α), interleukin 1 (IL-1), and interferon-γ (IFN-γ) are pivotal mediators in SE-induced toxic shock (6 ,7 ). High levels of these cytokines in serum are pathogenic and correlate with clinical symptoms of toxic shock (8 ,10 ).