title: Serum high mobility group box 1 is upregulated in myasthenia gravis.
abstract: OBJECTIVE
  High mobility group box 1 (HMGB1) functions as an inflammatory mediator and is implicated in the pathogenesis of various autoimmune diseases. Our primary aim is to determine whether HMGB1 is involved in the pathogenesis of myasthenia gravis (MG).
  
  
  METHODS
  Serum HMGB1 levels of 60 patients with anti-acetylcholine receptor (AChR) antibody-positive MG without immunosuppressive treatment and of 10 patients with anti-muscle-specific receptor tyrosine kinase (MuSK) antibody-positive MG were compared with those in 40 controls. We also investigated the potential correlation between serum HMGB1 levels and the clinical variables in patients with MG.
  
  
  RESULTS
  Serum HMGB1 levels in patients with anti-AChR antibody-positive MG were higher than those in controls (7.80 ± 7.47 vs 4.13 ± 2.55 ng/mL, p=0.004) and were decreased after treatment (p=0.051). Although not significant, patients with anti-MuSK antibody-positive MG showed higher serum HMGB1 levels than the controls (p=0.178). There were correlations between serum HMGB1 levels and phenotypes of anti-AChR antibody-positive MG: patients with generalised MG showed higher HMGB1 levels than those of patients with ocular MG (p=0.059) and controls (p=0.002); patients with thymoma showed higher HMGB1 levels than those without thymoma (p=0.094) and controls (p=0.001).
  
  
  CONCLUSIONS
  Serum HMGB1 is elevated in patients with MG and may play a key role in the inflammation of the neuromuscular junction.
authors.affiliation: Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Akiyuki
authors.initials: A
authors.lastname: Uzawa
authors.affiliation: Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan Department of Neurology, Neurology Chiba Clinic, Chiba, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Kawaguchi
authors.affiliation: Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kanai
authors.affiliation: Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Himuro
authors.affiliation: Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Satoshi
authors.identifier: http://orcid.org/0000-0002-4716-8578
authors.initials: S
authors.lastname: Kuwabara
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000032:analysis; D005260:Female; D024243:HMGB1 Protein / Q000096:biosynthesis* / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009157:Myasthenia Gravis / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D020794:Receptor Protein-Tyrosine Kinases / Q000276:immunology; D011950:Receptors, Cholinergic / Q000276:immunology; D015854:Up-Regulation / Q000235:genetics; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D024243:HMGB1 Protein; C585491:HMGB1 protein, human; D011950:Receptors, Cholinergic; C095714:MUSK protein, human; D020794:Receptor Protein-Tyrosine Kinases
keywords: CLINICAL NEUROLOGY; IMMUNOLOGY; MYASTHENIA; NEUROIMMUNOLOGY