May 1991
Volume 32, Issue 6
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Articles  |   May 1991
Ocular inflammation in MRL/Mp-lpr/lpr mice.
Author Affiliations
  • D A Jabs
    Wilmer Ophthalmological Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
  • R A Prendergast
    Wilmer Ophthalmological Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Investigative Ophthalmology & Visual Science May 1991, Vol.32, 1944-1947. doi:
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      D A Jabs, R A Prendergast; Ocular inflammation in MRL/Mp-lpr/lpr mice.. Invest. Ophthalmol. Vis. Sci. 1991;32(6):1944-1947.

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

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Abstract

A systemic autoimmune disease spontaneously developed in MRL/Mp-lpr/lpr (MRL/lpr) mice. The disease was characterized by vasculitis, lymphadenopathy, glomerulonephritis, and autoantibody formation. Among the many autoimmune lesions are focal ocular inflammatory infiltrates involving the choroid and sclera. Of 104 mice examined histologically, the sclera was most often involved, with 30% of mice 5 months of age or older having scleral lesions that were often centered around small arteries. The choroid was the second most frequently involved tissue, with focal inflammation developing in 16% of these mice. Immunohistologic analysis of the ocular infiltrates showed that most of the mononuclear cells seen were L3T4 + T cells (CD4+ helper T cells), suggesting that the process was largely T cell-mediated. Smaller numbers of B cells and Lyt 2+ T suppressor/cytotoxic cells were seen. No such lesions were seen in congenic MRL/Mp- +/+, (NZBxNZW) F1 hybrid mice, and control BALB/c mice; vasculitis did not develop in all of the mice. These results suggest that the ocular lesions in MRL/lpr mice may be a model for ocular involvement in patients who have systemic necrotizing vasculitis.

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