October 1989
Volume 30, Issue 10
Free
Articles  |   October 1989
Cryopexy enhances experimental autoimmune uveoretinitis (EAU) in rats.
Author Affiliations
  • R de Bara
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • M Kusuda
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • L Caspers-Velu
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • H Sanui
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • C C Chan
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • T Kuwabara
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • R B Nussenblatt
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
  • I Gery
    Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
Investigative Ophthalmology & Visual Science October 1989, Vol.30, 2165-2173. doi:
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    • Get Citation

      R de Bara, M Kusuda, L Caspers-Velu, H Sanui, C C Chan, T Kuwabara, R B Nussenblatt, I Gery; Cryopexy enhances experimental autoimmune uveoretinitis (EAU) in rats.. Invest. Ophthalmol. Vis. Sci. 1989;30(10):2165-2173.

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Abstract

Treatment of rat eyes with cryopexy enhanced the development of experimental autoimmune uveitis (EAU) in these eyes. The enhancement of EAU by cryopexy was particularly pronounced when the disease was induced by active immunization in rats of a low responder strain (Wistar Furth), or by adoptive transfer with lymphocytes sensitized against S-antigen. The disease enhancement was expressed by earlier onset of clinical symptoms and by more severe inflammatory changes. Histological examination of cryopexy-treated eyes showed focal necrosis and inflammation, confined to the affected sites. Immunohistochemical analysis of the inflammatory infiltration revealed it consists mainly of macrophages and T-lymphocytes of the helper and suppressor subsets. In addition, increased expression of class II antigens was observed in affected areas, on both inflammatory and resident ocular cells. Using electron microscopy and Evans blue angiography we could show breakdown of the blood-retinal barrier at the treated sites. Histological examination of eyes with EAU following cryopexy showed localization of the early inflammation at the injured site. The data are interpreted to suggest that the enhanced EAU in cryopexy-treated eyes is mainly due to the breakdown of the blood-retinal barrier, the accumulation of lymphoid cells and the increased expression of class II antigens, which facilitates antigen presentation.

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