October 1996
Volume 37, Issue 11
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Articles  |   October 1996
Anti-tumor necrosis factor alpha therapy suppresses the induction of experimental autoimmune uveoretinitis in mice by inhibiting antigen priming.
Author Affiliations
  • G Sartani
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • P B Silver
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • L V Rizzo
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • C C Chan
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • B Wiggert
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • G Mastorakos
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • R R Caspi
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Investigative Ophthalmology & Visual Science October 1996, Vol.37, 2211-2218. doi:
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      G Sartani, P B Silver, L V Rizzo, C C Chan, B Wiggert, G Mastorakos, R R Caspi; Anti-tumor necrosis factor alpha therapy suppresses the induction of experimental autoimmune uveoretinitis in mice by inhibiting antigen priming.. Invest. Ophthalmol. Vis. Sci. 1996;37(11):2211-2218.

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

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Abstract

PURPOSE: Experimental autoimmune uveoretinitis (EAU) serves as a model for several immune-mediated diseases that affect the eye in humans. Previous studies indicated that tumor necrosis factor alpha (TNF-alpha) has an important proinflammatory role in EAU and possibly in human uveitis. In this study, the authors investigated the effect of anti-TNF-alpha therapy on EAU in mice. METHODS: Experimental autoimmune uveoretinitis was induced in B10.A mice by immunization with interphotoreceptor retinoid-binding protein (IRBP). The mice were treated with 100 or 300 microliters rabbit antiserum or polyclonal antibodies to human TNF-alpha. The treatment spanned either the afferent or the efferent stage of EAU (days -1, 1, 3, 5, 7, or days 8, 10, 12, 14, 16, respectively). Control animals were injected with preimmune rabbit serum at the corresponding times or were not treated. Three weeks after immunization, EAU was assessed by clinical evaluation and by histopathology. Immunologic responses were assessed by delayed-type hypersensitivity (DTH), lymphocyte proliferation to IRBP, and relative abundance of IRBP-primed splenocytes. RESULTS: The treatment with rabbit anti-TNF-alpha serum significantly ameliorated disease when given during the afferent stage but had no effect when given during the efferent stage of EAU. The effect on DTH, lymphocyte proliferation, and abundance of antigen-reactive cells roughly paralleled the effect on disease. CONCLUSIONS: Neutralization of systemic TNF ameliorates EAU. The effectiveness of afferent treatment in comparison to the treatment during the efferent stage, together with the reduced proliferation and the reduced abundance of IRBP-responsive cells, suggest that interference with afferent-acting processes such as antigen priming is important to achieve protection from EAU by anti-TNF treatment.

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