title: The humoral response in the pathogenesis of gluten ataxia.
abstract: OBJECTIVE
  To characterize humoral response to cerebellum in patients with gluten ataxia.
  
  
  BACKGROUND
  Gluten ataxia is a common neurologic manifestation of gluten sensitivity.
  
  
  METHODS
  The authors assessed the reactivity of sera from patients with gluten ataxia (13), newly diagnosed patients with celiac disease without neurologic dysfunction (24), patients with other causes of cerebellar degeneration (11), and healthy control subjects (17) using indirect immunocytochemistry on human cerebellar and rat CNS tissue. Cross-reactivity of a commercial IgG antigliadin antibody with human cerebellar tissue also was studied.
  
  
  RESULTS
  Sera from 12 of 13 patients with gluten ataxia stained Purkinje cells strongly. Less intense staining was seen in some but not all sera from patients with newly diagnosed celiac disease without neurologic dysfunction. At high dilutions (1:800) staining was seen only with sera from patients with gluten ataxia but not in control subjects. Sera from patients with gluten ataxia also stained some brainstem and cortical neurons in rat CNS tissue. Commercial anti-gliadin antibody stained human Purkinje cells in a similar manner. Adsorption of the antigliadin antibodies using crude gliadin abolished the staining in patients with celiac disease without neurologic dysfunction, but not in those with gluten ataxia.
  
  
  CONCLUSIONS
  Patients with gluten ataxia have antibodies against Purkinje cells. Antigliadin antibodies cross-react with epitopes on Purkinje cells.
authors.affiliation: Department of Clinical Neurology, The Royal Hallamshire Hospital, Sheffield, UK. m.hadjivassiliou@sheffield.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Hadjivassiliou
authors.forename: S
authors.initials: S
authors.lastname: Boscolo
authors.forename: G A B
authors.initials: GA
authors.lastname: Davies-Jones
authors.forename: R A
authors.initials: RA
authors.lastname: Grünewald
authors.forename: T
authors.initials: T
authors.lastname: Not
authors.forename: D S
authors.initials: DS
authors.lastname: Sanders
authors.forename: J E
authors.initials: JE
authors.lastname: Simpson
authors.forename: E
authors.initials: E
authors.lastname: Tongiorgi
authors.forename: C A
authors.initials: CA
authors.lastname: Williamson
authors.forename: N M
authors.initials: NM
authors.lastname: Woodroofe
mesh_terms: D000368:Aged; D000818:Animals; D000917:Antibody Formation; D001259:Ataxia / Q000276:immunology*; D064026:Calbindins; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology; D005260:Female; D005903:Gliadin / Q000737:chemistry / Q000235:genetics; D005983:Glutens / Q000009:adverse effects* / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000235:genetics / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011689:Purkinje Cells / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D064030:S100 Calcium Binding Protein G
chemical_list: D064026:Calbindins; D007074:Immunoglobulin G; D064030:S100 Calcium Binding Protein G; D005983:Glutens; D005903:Gliadin