title: Interleukin 23 in acute inflammatory demyelination of the peripheral nerve.
abstract: BACKGROUND
  Interleukin (IL) 23, a newly identified heterodimeric proinflammatory cytokine and a novel IL-12 family member comprising the p40 subunit of IL-12 but a different p19 subunit, has been reported to preferentially act on memory T cells and play an important role during cellular immune responses. Recent evidence suggests that IL-23 rather than IL-12 is critically involved in the pathogenesis of various immune-mediated disorders.
  
  
  OBJECTIVE
  To determine the role of IL-23p19 during the course of acute immune-mediated demyelinating diseases of the peripheral nervous system.
  
  
  METHODS
  The sequential RNA expression of IL-23p19 in sciatic nerves from rats with experimental autoimmune neuritis, an animal model of the human Guillain-Barré syndrome (GBS), was analyzed by semiquantitative reverse transcriptase-polymerase chain reaction. Expression and distribution patterns of IL-23p19 protein were studied in sural nerve biopsies and cerebrospinal fluid samples from 5 patients with classical Guillain-Barré syndrome and 5 controls with noninflammatory neuropathies using immunohistochemistry and immunoblotting, respectively.
  
  
  RESULTS
  We found IL-23p19 RNA to be up-regulated prior to the onset of first clinical symptoms with peak expression levels preceding maximum disease severity during experimental autoimmune neuritis. In patients, IL-23p19 protein was detectable in cerebrospinal fluid samples from patients with Guillain-Barré syndrome, and endoneurial macrophages were identified as the cellular source of IL-23p19 in sural nerve biopsies.
  
  
  CONCLUSIONS
  Our present data indicate that IL-23 may play an important role during the early effector phase in immune-mediated demyelination of the peripheral nerve.
authors.affiliation: Department of Neurology, Research Group for Clinical and Experimental Neuroimmunology, Heinrich-Heine-University, Düsseldorf, Germany.
authors.forename: Wei
authors.initials: W
authors.lastname: Hu
authors.forename: Thomas
authors.initials: T
authors.lastname: Dehmel
authors.forename: Jaana
authors.initials: J
authors.lastname: Pirhonen
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Hartung
authors.forename: Bernd C
authors.initials: BC
authors.lastname: Kieseier
mesh_terms: D000818:Animals; D015153:Blotting, Western / Q000379:methods; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique / Q000379:methods; D020275:Guillain-Barre Syndrome / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D053759:Interleukin-23; D053760:Interleukin-23 Subunit p19; D007378:Interleukins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D009444:Neuritis, Autoimmune, Experimental / Q000378:metabolism* / Q000473:pathology; D010525:Peripheral Nerves / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013997:Time Factors
chemical_list: C508840:IL23A protein, human; C508842:Il23a protein, rat; D053759:Interleukin-23; D053760:Interleukin-23 Subunit p19; D007378:Interleukins; D012333:RNA, Messenger