Kinetics and Specificity of Fas Ligand Induction in Toxic Epidermal Necrolysis

Recent advances in the genetics and immunology of Stevens-Johnson syndrome and toxic epidermal necrosis

“…Viard et al reported that FasL distributes on the keratinocyte cell surface, and soluble FasL (sFasL) presented with a high level in the serum of TEN patients. A consistent finding of the increased sFasL expression after the onset of skin damage in TEN has been reported by Chang et al [51]. However, the proposed role of FasL in the induction of keratinocyte apoptosis in SJS/TEN was questioned by other studies.…”

Toxic epidermal necrolysis

“…116,117 The increased serum levels of sFasL observed in TEN patients may be caused by the action of MPs at the keratinocyte cell surface. 114 Consistent with this idea is a clinical observation made by Chang et al 118 Serum levels of sFasL from a 42-year-old male with antibiotic-induced TEN were measured daily. A marked rise in sFasL levels occurred approximately 24 to 48 hours after the onset of major skin damage.…”

“…A marked rise in sFasL levels occurred approximately 24 to 48 hours after the onset of major skin damage. 118 This observation suggests that sFasL does not cause keratinocyte apoptosis, but rather that it is a byproduct of FasL expressed by keratinocytes. Not all investigators have been able to duplicate Viard's model.…”

Recovered Patients with Stevens–Johson Syndrome and Toxic Epidermal Necrolysis Maintain Long-Lived IFN-γ and sFasL Memory Response

“…In patients with SJS and TEN, sFasL level in serum is increased significantly before or after onset of skin damage [23], [24], [25]. PBMCs from patients with SJS and TEN secrete significant amounts of sFasL in the acute stage after stimulation with causal drugs, which subsequently induce keratinocyte apoptosis in a dose-dependent manner [8].…”