Tumor necrosis factor-α in Guillain-Barré syndrome, friend or foe?

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.

KEYWORDS:

• Experimental autoimmune neuritis
• Guillain-Barré syndrome
• TNF-α
• therapeutic target

Article highlights

• The TNF-α family members, including tmTNF and solTNF, bear pro-inflammatory or anti-inflammatory properties by binding to TNFR1 or TNFR2.

• TNF-α gene polymorphisms are associated with the risk of GBS, serum levels of TNF-α as well as the subtypes of GBS.

• The TNF-α mainly plays a pro-inflammatory role in GBS and EAN. However, anti-inflammatory role of TNF-α is also reported.

• A number of biological treatments are proved to be effective on EAN via modulating the expression of TNF-α.

• Further investigations are warranted to explore the role of TNF-α when it binds to distinct receptors, the gene polymorphism of TNF-α, and the cross-talk between TNF-α and other immune factors, so as to elucidate the pathogenesis of GBS.

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Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

The work was supported by grants from the Elite PHD Program of Bethune Health Science Center, Jilin University (no. 470110000421).