The role of chemokines in guillain–barré syndrome


  • This study was supported by the National Institutes of Health [T32 CA96520 to S.C., and R21 NS073702 (2011–2013), R21 NS078226 (2012–2014), and R01 NS075212 (2012–2017) to E.E.U.] and an award from the Guillain–Barré syndrome/Chronic Inflammatory Demyelinating Polyradiculoneuropathy Foundation International (2010–2012).

  • Disclosure: The content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health.

Correspondence to: E.E. Ubogu; e-mail:


Introduction: Chemokines and their receptors are important mediators of inflammation. Guillain–Barré syndrome (GBS) is the most common cause of acute paralysis worldwide. Despite current treatments, outcomes are suboptimal. Specific chemokine receptor antagonists have the potential to be efficacious against pathogenic leukocyte trafficking in GBS. Methods: A 36-year literature review was performed to summarize available data on chemokine expression in GBS and its representative animal model, experimental autoimmune neuritis (EAN). Results: Although there were a few observational human and animal studies demonstrating chemokine ligand/receptor expression in GBS and EAN, in vitro and in vivo functional studies using gene knockouts, neutralizing antibodies, or small molecular antagonists were limited. CCL2–CCR2, CCL5–CCR5, and CXCL10–CXCR3 have been most strongly implicated in EAN and GBS pathogenesis, providing targets for molecular blockade. Conclusions: Preclinical human in vitro and in vivo EAN studies are needed to evaluate the potential efficacy of chemokine signaling inhibition in GBS. Muscle Nerve 48: 320–330, 2013