title: Are Th17 cells and their cytokines a therapeutic target in Guillain-Barré syndrome?
abstract: BACKGROUND
  Guillain-Barré syndrome (GBS) is an immune-mediated inflammatory disorder of the peripheral nervous system (PNS). Experimental autoimmune neuritis (EAN) is a useful animal model for studying GBS. Currently, GBS remains a life-threatening disorder and more effective therapeutic strategies are in urgent need.
  
  
  METHODS
  Accumulating evidence has revealed that T helper (Th) 17 cells and their cytokines are pathogenic in GBS/EAN. Drugs attenuated clinical signs of GBS/EAN, in part, by decreasing Th17 cells or IL-17A. Th17 cells and their cytokines might be potential therapeutic targets. Approaches targeting Th17 cells or their cytokines are in development in treating Th17 cells-involved disorders. In this review, we summarize the up-to-date knowledge on roles of Th17 cells and their cytokines in GBS/EAN, as well potential approaches targeting Th17 cells and their cytokines as clinical applications.
  
  
  CONCLUSIONS
  As Th17 cells produce different sets of pro-inflammatory cytokines and Th17-related cytokines are not exclusively produced by Th17 cells, targeting Th17 cell development may be superior to blocking a single Th17 cytokine to treat Th17 cells-involved disorders. Considering the essential role of retinoic acid-related orphan receptor γT (RORγT) and IL-23 in Th17 cell development, RORγT inhibitors or IL-23 antagonists may provide better clinical efficacy in treating GBS/EAN.
authors.affiliation: a 1 The First Hospital of Jilin University, Neuroscience Center, Department of Neurology , Changchun, China ; drzhl@hotmail.com.
authors.forename: Xiujuan
authors.initials: X
authors.lastname: Wu
authors.affiliation: a 1 The First Hospital of Jilin University, Neuroscience Center, Department of Neurology , Changchun, China ; drzhl@hotmail.com.
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.affiliation: a 1 The First Hospital of Jilin University, Neuroscience Center, Department of Neurology , Changchun, China ; drzhl@hotmail.com.
authors.forename: Kangding
authors.initials: K
authors.lastname: Liu
authors.affiliation: a 1 The First Hospital of Jilin University, Neuroscience Center, Department of Neurology , Changchun, China ; drzhl@hotmail.com.|b 2 Karolinska Institute, Department of Neurobiology, Care Sciences and Society , Stockholm, Sweden.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
authors.affiliation: a 1 The First Hospital of Jilin University, Neuroscience Center, Department of Neurology , Changchun, China ; drzhl@hotmail.com.|b 2 Karolinska Institute, Department of Neurobiology, Care Sciences and Society , Stockholm, Sweden.
authors.forename: Hong-Liang
authors.initials: HL
authors.lastname: Zhang
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology*; D015195:Drug Design; D020275:Guillain-Barre Syndrome / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D006801:Humans; D053759:Interleukin-23 / Q000037:antagonists & inhibitors; D058990:Molecular Targeted Therapy; D009444:Neuritis, Autoimmune, Experimental / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000037:antagonists & inhibitors; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D053759:Interleukin-23; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3
keywords: Guillain–Barré syndrome; T helper cell; Th17 cell; cytokine; experimental autoimmune neuritis