title: Oral administration of interferon-beta suppresses experimental autoimmune uveoretinitis.
abstract: BACKGROUND
  The oral administration of type I interferons (IFNs) have been reported to reduce severity of inflammation in several animal models of autoimmune disease. This study examined whether oral administration of IFN-beta is capable of modulating inflammation in experimental autoimmune uveoretinitis (EAU).
  
  
  METHODS
  EAU was induced in rats by immunization with interphotoreceptor retinoid-binding protein (IRBP) emulsified in complete Freund's adjuvant. Rats were treated with either varying doses (10(2), 10(3), 10(4) or 10(5)IU) of mouse recombinant IFN-beta or phosphate-buffered saline for control, via direct oropharyngeal application once a day for 28 days starting 7 days before IRBP immunization. Intraocular inflammation was assessed by slit-lamp biomicroscopy and histopathological examination. Spleen cell proliferation response and cytokine production under IRBP stimulation were assessed. Spleen cell subpopulations were also measured.
  
  
  RESULTS
  IFN-beta at doses of either 10(4) or 10(5) IU significantly reduced both the clinical and histopathological severity of EAU. Spleen cell proliferation and IFN-gamma production from rats treated with 10(4) IU IFN-beta were significantly decreased compared with controls. Furthermore, the proportion of both NK cells and NKT cells in the spleen of rats treated with IFN-beta was increased compared with controls.
  
  
  CONCLUSIONS
  These results suggest that the oral administration of IFN-beta reduces inflammation in IRBP-mediated EAU and that the mechanism of this action may involve NK cells and NKT cells.
authors: Department of Ophthalmology, Tokyo Medical University Hospital, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. jun-s@qc4.so-net.ne.jp
authors: Jun
authors: J
authors: Suzuki
authors: Jun-Ichi
authors: J
authors: Sakai
authors: Annabelle A
authors: AA
authors: Okada
authors: Eiko
authors: E
authors: Takada
authors: Masahiko
authors: M
authors: Usui
authors: Junichiro
authors: J
authors: Mizuguchi
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D005136:Eye Proteins; D005260:Female; D005434:Flow Cytometry; D007370:Interferon Type I / Q000008:administration & dosage*; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D051381:Rats; D011917:Rats, Inbred Lew; D011994:Recombinant Proteins; D012173:Retinitis / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D012177:Retinol-Binding Proteins; D013154:Spleen / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology; D014605:Uveitis / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D005136:Eye Proteins; D007370:Interferon Type I; D011994:Recombinant Proteins; D012177:Retinol-Binding Proteins; D000099214:Retinol-Binding Proteins, Interstitial