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Cytotoxic Proteins and Therapeutic Targets in Severe Cutaneous Adverse Reactions

by Shih-Chi Su 1 and Wen-Hung Chung 1,2,*
1
Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospitals, Taipei, Linkou, and Keelung, 33305, Taiwan
2
College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
*
Author to whom correspondence should be addressed.
Toxins 2014, 6(1), 194-210; https://doi.org/10.3390/toxins6010194
Received: 28 November 2013 / Revised: 20 December 2013 / Accepted: 27 December 2013 / Published: 3 January 2014
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. View Full-Text
Keywords: Stevens-Johnson syndrome; toxic epidermal necrosis; granulysin; perforin; granzyme B; Fas/Fas ligand Stevens-Johnson syndrome; toxic epidermal necrosis; granulysin; perforin; granzyme B; Fas/Fas ligand
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Su, S.-C.; Chung, W.-H. Cytotoxic Proteins and Therapeutic Targets in Severe Cutaneous Adverse Reactions. Toxins 2014, 6, 194-210.

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