Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand
Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand
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DOI:
10.1016/s0002-9440(10)64284-8
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发表时间:
2003-05-01
影响因子:
6
通讯作者:
Shimizu, H
中科院分区:
文献类型:
--
作者:
Abe, R;Shimizu, T;Shimizu, H
The pathogeneses of toxic epidermal necrolysis (TEN) and Stevens Johnson syndrome (SJS), both severe blistering diseases usually associated with drug intake, are not fully elucidated. Histologically, both TEN and SJS are characterized by extensive keratinocyte apoptosis. Previous studies have shown that keratinocyte apoptosis in TEN and SJS was induced by a suicidal interaction between Fas and Fas ligand (FastL), which are both expressed by keratinocytes. However, our preliminary examinations demonstrated that FasL is hardly detected on keratinocytes. We hypothesized that soluble FasL (sFasL) is secreted by peripheral blood mononuclear cells (PBMCs), and this interacts with the Fas expressed on keratinocytes in TEN and SJS. To justify this hypothesis, we investigated whether sFasL secreted by PBMCs could induce the keratinocyte apoptosis in TEN and SJS. Enzyme-linked immunosorbent assay analysis demonstrated that there was no significant sFasL increase in any samples of healthy controls (