April 1994
Volume 35, Issue 5
Free
Articles  |   April 1994
Suppression of experimental uveitis with monoclonal antibodies to ICAM-1 and LFA-1.
Author Affiliations
  • E Uchio
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • M Kijima
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • S Tanaka
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • S Ohno
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
Investigative Ophthalmology & Visual Science April 1994, Vol.35, 2626-2631. doi:
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    • Get Citation

      E Uchio, M Kijima, S Tanaka, S Ohno; Suppression of experimental uveitis with monoclonal antibodies to ICAM-1 and LFA-1.. Invest. Ophthalmol. Vis. Sci. 1994;35(5):2626-2631.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: Intercellular adhesion molecule-1 (ICAM-1), which is one of the ligands for lymphocyte function associated antigen-1 (LFA-1), plays an important role in immune responses. To examine whether ICAM-1 and LFA-1 are involved in the pathogenesis of experimental autoimmune uveoretinitis (EAU), the authors investigated the therapeutic effect of anti-ICAM-1 monoclonal antibody (mAb) 1A29 and anti-LFA-1 alpha chain mAb WT.1 on retinal soluble antigen (S-Ag) and Freund's complete adjuvant (FCA)-induced EAU in rats. METHODS: After immunization with S-Ag and FCA, rats were intraperitoneally injected with a monoclonal antibody, anti-ICAM-1 mAb 1A29 or anti-LFA-1 alpha chain mAb or control Ab, at 1.0 mg/kg body weight, according to the treatment schedule. Inflammation was examined clinically and histologically. Proliferative responses of splenocytes to S-Ag were also examined. RESULTS: The development of EAU could be completely prevented by the administration of 1A29, 1.0 mg/kg, twice a week from day 0 to day 14, but was only partially suppressed by WT.1. However, semiweekly administration of 1A29 from day 0 to day 7, or from day 10 to day 17, did not suppress EAU. CONCLUSIONS: These findings indicate that ICAM-1, LFA-1-dependent pathways are involved in the pathogenesis of EAU. In addition, these pathways seem to be required for both the induction and the development of this disease.

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