| Literature DB >> 27817222 |
Ying Wang1, Jingdian Zhang1, Peijuan Luo2, Jie Zhu1,3, Jiachun Feng1, Hong-Liang Zhang1.
Abstract
INTRODUCTION: Guillain-Barré syndrome (GBS) is an immune-mediated disorder in the peripheral nervous system (PNS), and experimental autoimmune neuritis (EAN) serves as an animal model of GBS. TNF-α plays an important role in the pathogenesis of GBS and is a potential therapeutic target of GBS. Areas covered: 'TNF-α' and 'Guillain-Barré syndrome' were the keywords used to search for related publications on Pubmed. By binding to different TNF receptors, TNF-α bears distinct immune properties. TNF-α gene polymorphisms are associated with the features of GBS. The major role of TNF-α in GBS/EAN is to aggravate inflammation; however, data from several studies indicated a protective role of TNF-α. Multiple lines of evidence point to TNF-α as a potential therapeutic target for GBS. However, such clinical trials are scarce in that GBS per se is a probable side effect of anti-TNF-α treatment. Expert opinion: TNF-α plays a dual role in GBS and EAN, and is a potential therapeutic target on GBS/EAN.Entities:
Keywords: Experimental autoimmune neuritis; Guillain-Barré syndrome; TNF-α; therapeutic target
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Year: 2016 PMID: 27817222 DOI: 10.1080/14728222.2017.1258402
Source DB: PubMed Journal: Expert Opin Ther Targets ISSN: 1472-8222 Impact factor: 6.902