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Interferon beta normalizes suppressor cell function in dysimmune neuropathies.

Abstract
We found a defective suppressor cell function in vitro both in idiopathic chronic inflammatory demyelinating polyneuropathy and in paraproteinemic neuropathy with antibodies to sulfated glucuronyl paragloboside. In the presence of interferon beta, suppressor cell function was normalized. Our results suggest that a decreased suppressor cell function plays a pathogenetic role in dysimmune neuropathies. Interferon beta might represent an adjunctive therapy in CIDP both acting on a defective blood-nerve barrier and normalizing an otherwise defective suppressor cell function.
AuthorsGiovanna De Luca, Alessandra Lugaresi, Carla Iarlori, Fabio Marzoli, Antonino Uncini, Domenico Gambi
JournalJournal of neuroimmunology (J Neuroimmunol) Vol. 82 Issue 1 Pg. 1-4 (Feb 1998) ISSN: 0165-5728 [Print] Netherlands
PMID9526839 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antibodies, Monoclonal
  • Globosides
  • Immunoglobulin M
  • Myelin-Associated Glycoprotein
  • Recombinant Proteins
  • sulfate-3-glucuronyl paragloboside
  • Interferon-beta
Topics
  • Adolescent
  • Adult
  • Aged
  • Antibodies, Monoclonal (blood)
  • Child
  • Demyelinating Diseases (immunology, therapy)
  • Female
  • Globosides (immunology)
  • Humans
  • Immunoglobulin M (blood)
  • Interferon-beta (administration & dosage)
  • Male
  • Middle Aged
  • Myelin-Associated Glycoprotein (immunology)
  • Paraproteinemias (immunology, therapy)
  • Peripheral Nervous System Diseases (immunology, therapy)
  • Polyneuropathies (immunology, therapy)
  • Recombinant Proteins (administration & dosage)

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