September 15, 2014

Cytotoxic proteins and therapeutic targets in severe cutaneous adverse reactions

Review

Cytotoxic Proteins and Therapeutic Targets in Severe Cutaneous Adverse Reactions

 1email and  1,2,email

Received: 28 November 2013; in revised form: 20 December 2013 / Accepted: 27 December 2013 / Published: 3 January 2014
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract: 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.
Keywords: Stevens-Johnson syndrome; toxic epidermal necrosis; granulysin; perforin; granzyme B; Fas/Fas ligand


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