text: SJS, like toxic epidermal necrolysis and erythema multiforme, are characterized by confluent epidermal necrosis with minimal associated inflammation. The acuity is apparent from the (normal) basket weave-like pattern of the stratum corneum. The exact pathogenesis of SJS/TEN is not completely understood. However, It is believed that SJS/TEN is immune-mediated and the result of an MHC Class-I restricted T-cell mediated cytotoxic reaction to drug antigens in keratinocytes leading to apoptosis. Drug antigens bind to MHC-I and T cell Receptors (TCR) leading to the clonal proliferation of the drug-specific cytotoxic T cells. On the activation of these T cells, various cytotoxic signals, including Fas/Fas ligand, perforin/granzyme B, and granulysin, are known to be responsible for mediating the damages in skin lesions and the subsequent worsening of the disease.
option_0: Stevens-Johnson syndrome pathophysiology
option_1: Staphylococcal scalded skin syndrome pathophysiology
option_2: Anaphylaxis pathophysiology
option_3: Stevens-Johnson syndrome risk factors
option_4: Herpes simplex pathophysiology
option_5: Stevens-Johnson syndrome classification
option_6: Stevens-Johnson syndrome laboratory findings
option_7: Cellulitis pathophysiology