September 1988
Volume 29, Issue 9
Free
Articles  |   September 1988
Murine models of Sjögren's syndrome. Immunohistologic analysis of different strains.
Author Affiliations
  • D A Jabs
    Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • R A Prendergast
    Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Investigative Ophthalmology & Visual Science September 1988, Vol.29, 1437-1443. doi:
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      D A Jabs, R A Prendergast; Murine models of Sjögren's syndrome. Immunohistologic analysis of different strains.. Invest. Ophthalmol. Vis. Sci. 1988;29(9):1437-1443.

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Abstract

Lacrimal gland inflammation develops in several strains of autoimmune mice, including MRL/Mp-lpr/lpr (MRL/lpr), MRL/Mp-+/+ (MRL/+), and NZBxNZW F1 hybrids (NZB/W). These mice all develop an autoimmune disease characterized by glomerulonephritis and autoantibody formation, but each strain has unique clinical features and immunologic abnormalities. Previous studies have suggested that the intrinsic immunologic defect in MRL/lpr mice may be at the level of T cells, while in NZB/W mice it appears to be B cell-mediated. Immunohistologic analysis of the lacrimal gland lesions was performed on all three strains. Although T cells predominated (MRL/lpr 85%, MLR/+ 78%, and NZB/W 57%), differences in the immunohistologic profiles did exist. NZB/W mice had a significantly higher percentage of B cells (33% vs. 10% for MRL/lpr and 13% for MRL/+) and a correspondingly lower percentage of T cells. MRL/lpr mice differed from MRL/+ mice in that they exhibited a significantly higher percentage of helper T cells (63% vs. 49%) and a lower percentage of suppressor/cytotoxic T cells (14% vs. 30%). Class II antigen expression could be detected on the mononuclear cells at inflammatory sites within the lacrimal glands of all three strains, suggesting T cell activation and an active autoimmune immunologic event occurring in the lacrimal gland.

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