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Oral administration of interferon-beta suppresses experimental autoimmune uveoretinitis
Jun Suzuki1, Jun-Ichi Sakai, Annabelle A Okada
1Department of Ophthalmology, Tokyo Medical University Hospital, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. jun-s@qc4.so-net.ne.jp
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.
Conclusion:
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.