Epidermal Apoptotic Cell Death in Erythema Multiforme and Stevens-Johnson Syndrome

Toxic Epidermal Necrolysis : A Case Report

“…Other authors have reported similar results with cyclosporin [5]. Cyclosporin inhibits the principal cellular population involved in the pathogenesis of TEN (activated T-lymphocytes, macrophages, keratinocytes), interferes with the metabolism of tumour necrosis factor (TNF), and possesses an anti-apoptosis property [6]. The effectiveness of cyclosporin could be due to its capacity to interrupt the disease evolution and allowing early re-epithelialisation of the cutaneous surfaces affected.…”

Cytotoxic Molecule Expression and Epithelial Cell Apoptosis in Oral and Cutaneous Lichen Planus

“…27 Lymphocytes expressing granzyme B, perforin, or both have been demonstrated in other diseases associated with basal epidermal cell damage, such as drug eruptions 28 and Stevens-Johnson syndrome. 29 We evaluated the degree of cytotoxic cell infiltrate in a series of OLP and CLP (characterized by similar degree of inflammatory activity according to Ragaz and Ackerman 17 and van der Meij and van der Waal 18 ) using the Tia-1 antigens and the expression of perforin and granzyme B, which are known to be expressed specifically by activated cytotoxic lymphocytes and to trigger cooperatively the death of target cells. In addition, the amount of epithelial cell death was studied by using the ssDNA technique, which detects early stages of cell apoptosis.…”

Erythema multiforme, Stevens–Johnson syndrome and toxic epidermal necrolysis: a comparative review

“…Interestingly, the pattern of ICAM‐1 expression differs in EM, lichen planus and systemic lupus erythematosus (SLE), reflecting the distribution of the targeted keratinocytes in each disease . Apoptosis is mediated by exocytosis of the protease contents of the cytolytic granules from CD8 + T lymphocytes, NK cells and other innate T cells . Granzymes enter the target cell through transient pores induced by perforin and trigger intrinsic apoptosis by both caspase‐dependent and ‐independent mechanisms.…”