Although intact TSST1 causes lethal shock in vivo, the individual domains of this molecule may have therapeutic potential: the N-terminal domain to antagonize lymphocyte activation and TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimulate antitumor responses without MHC II binding.
Given that etanercept can be used to successfully treat SJS/TEN and TNF-alpha levels are elevated in TSS, if a dermatologist chooses to treat TEN with etanercept, consideration of TSS on the differential should not necessarily exclude etanercept as a reasonable treatment option.
Major histocompatibility complex (MHC) class II engagement by toxic shock syndrome toxin 1 (TSST-1) transduces signals leading to proinflammatory cytokine gene expression (tumor necrosis factor alpha [TNF-alpha]) in human monocytes.