Document Detail

Interleukin 23 in acute inflammatory demyelination of the peripheral nerve.
MedLine Citation:
PMID:  16769867     Owner:  NLM     Status:  MEDLINE    
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. DESIGN: 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. CONCLUSION: 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.
Wei Hu; Thomas Dehmel; Jaana Pirhonen; Hans-Peter Hartung; Bernd C Kieseier
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Archives of neurology     Volume:  63     ISSN:  0003-9942     ISO Abbreviation:  Arch. Neurol.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-13     Completed Date:  2006-07-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372436     Medline TA:  Arch Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  858-64     Citation Subset:  AIM; IM    
Department of Neurology, Research Group for Clinical and Experimental Neuroimmunology, Heinrich-Heine-University, Düsseldorf, Germany.
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MeSH Terms
Blotting, Western / methods
Disease Models, Animal
Fluorescent Antibody Technique / methods
Guillain-Barre Syndrome / metabolism*,  pathology
Interleukin-23 Subunit p19
Interleukins / genetics,  metabolism*
Neuritis, Autoimmune, Experimental / metabolism*,  pathology
Peripheral Nerves / metabolism*,  pathology
RNA, Messenger / metabolism
Rats, Inbred Lew
Reverse Transcriptase Polymerase Chain Reaction / methods
Time Factors
Reg. No./Substance:
0/IL23A protein, human; 0/Il23a protein, rat; 0/Interleukin-23; 0/Interleukin-23 Subunit p19; 0/Interleukins; 0/RNA, Messenger

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