ABSTRACT
Introduction: Macrophage migration inhibitory factor (MIF) plays an important role in the pathogenesis of Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN), which may offer an opportunity for the development of the novel therapeutic strategies for GBS.
Areas covered: ‘macrophage migration inhibitory factor’ and ‘Guillain-Barré syndrome’ were used as keywords to search for related publications on Pub-Med, National Center for Biotechnology Information (NCBI), USA. MIF is involved in the etiology of various inflammatory and autoimmune disorders. However, the roles of MIF in GBS and EAN have not been summarized in the publications we identified. Therefore, in this review, we described and analyzed the major roles of MIF in GBS/EAN. Primarily, this molecule aggravates the inflammatory responses in this disorder. However, multiple studies indicated a protective role of MIF in GBS. The potential of MIF as a therapeutic target in GBS has been recently demonstrated in experimental and clinical studies, although clinical trials have been unavailable to date.
Expert opinion: MIF plays a critical role in the initiation and progression of GBS and EAN, and it may represent a potential therapeutic target for GBS.
Article highlights
MIF is involved in the etiology of various inflammatory and autoimmune disorders.
MIF plays a critical role in the initiation and progression of both GBS and EAN through aggravating inflammatory responses in these disorders.
However, it is also indicated a protective role of MIF in GBS. Thus, further investigations are warranted to explore the role of MIF in GBS.
The therapeutic effects of MIF inhibitors have been demonstrated in several models of autoimmune diseases, including EAN.
MIF may represent a potential therapeutic target for GBS in the future.
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Declaration of interest
The authors have no other 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 apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose