Cytotoxic Proteins and Therapeutic Targets in Severe Cutaneous Adverse Reactions

被引:43
作者
Su, Shih-Chi [1 ,2 ,3 ]
Chung, Wen-Hung [1 ,2 ,3 ,4 ]
机构
[1] Chang Gung Mem Hosp, Dept Dermatol, Drug Hypersensit Clin & Res Ctr, Taipei 33305, Taiwan
[2] Chang Gung Mem Hosp, Dept Dermatol, Drug Hypersensit Clin & Res Ctr, Linkou 33305, Taiwan
[3] Chang Gung Mem Hosp, Dept Dermatol, Drug Hypersensit Clin & Res Ctr, Keelung 33305, Taiwan
[4] Chang Gung Univ, Coll Med, Taoyuan 33302, Taiwan
关键词
Stevens-Johnson syndrome; toxic epidermal necrosis; granulysin; perforin; granzyme B; Fas/Fas ligand; TOXIC EPIDERMAL NECROLYSIS; STEVENS-JOHNSON-SYNDROME; TUMOR-NECROSIS-FACTOR; DOSE INTRAVENOUS IMMUNOGLOBULINS; CYTOCHROME-C RELEASE; GRANZYME-B; FACTOR-ALPHA; FAS LIGAND; INTERFERON-GAMMA; T-CELLS;
D O I
10.3390/toxins6010194
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Severe cutaneous adverse reactions (SCARs), such as Stevens-Johnson syndrome (SJS) and toxic epidermal necrosis (TEN), are rare but life-threatening conditions induced mainly by a variety of drugs. Until now, an effective treatment for SJS/TEN still remains unavailable. Current studies have suggested that the pathobiology of drug-mediated SJS and TEN involves major histocompatibility class (MHC) I-restricted activation of cytotoxic T lymphocytes (CTLs) response. This CTLs response requires several cytotoxic signals or mediators, including granulysin, perforin/granzyme B, and Fas/Fas ligand, to trigger extensive keratinocyte death. In this article, we will discuss the cytotoxic mechanisms of severe cutaneous adverse reactions and their potential applications on therapeutics for this disease.
引用
收藏
页码:194 / 210
页数:17
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