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 V_β 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).