[Recent progress in research of pathogeneses of Stevens-Johnson syndrome and toxic epidermal necrolysis].

Stevens-Johnson syndrome(SJS)and toxic epidermal necrolysis(TEN)are life-threatening cutaneous adverse drug reactions that induce widespread epidermal necrosis. Ocular and cutaneous diseases are common chronic sequelae of SJS and TEN. Several concepts have been proposed to explain the pathogenesis of severe cutaneous adverse drug reactions. Recent advances in genetic, pharmacogenomics and immunologic studies have provided evidences of genetic predispositions, drug metabolism and cytokines related to SJS and TEN. With regard to keratinocyte death, several cell death mediators, such as Fas/FasL, granulysin and TNF, have been proposed to play an important role in the pathogeneses of SJS and TEN. A subset of T lymphocytes, including regulatory T cells, may also play a role. This review summarizes the pathogeneses of SJS and TEN mainly from the aspects of genetic susceptibilities, drug metabolism, and immune cells and cytokines. (Chin J Ophthalmol, 2016, 52: 708-713).