May 1992
Volume 33, Issue 6
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Articles  |   May 1992
Experimental autoimmune dacryoadenitis: purification and characterization of a lacrimal gland antigen.
Author Affiliations
  • S H Liu
    Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • D H Zhou
    Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Investigative Ophthalmology & Visual Science May 1992, Vol.33, 2029-2036. doi:
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      S H Liu, D H Zhou; Experimental autoimmune dacryoadenitis: purification and characterization of a lacrimal gland antigen.. Invest. Ophthalmol. Vis. Sci. 1992;33(6):2029-2036.

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

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Abstract

A soluble lacrimal gland antigen (LG-Ag) capable of inducing experimental autoimmune dacryoadenitis (EAD) in SJL/J mice has been purified from bovine lacrimal gland extracts by a combination of ion exchange and gel-filtration chromatography. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed a single band with a mobility corresponding to a molecular weight of 45,000 daltons. Antibodies raised in guinea pigs against purified LG-Ag were used to confirm the tissue-specificity and to assess the cellular localization of LG-Ag within tissues. Anti-LG-Ag serum reacted with the crude lacrimal gland extracts but not with the extracts of bovine submaxillary gland, parotid gland, or retina. As shown by immunofluorescent staining, LG-Ag appeared to be localized on the murine lacrimal ductal epithelial cells but was lacking in the salivary ducts. LG-Ag induced EAD that was characterized by infiltration of mononuclear cells around the ducts and associated vasculature, accompanied by extensive damage of the acinar cells. The lesions induced were tissue-specific, in that SJL/J mice immunized with LG-Ag had intense lymphocytic infiltrates in lacrimal gland, but had no significant lesions in their salivary and harderian glands. The availability of a purified LG antigen can facilitate the further analysis of pathogenetic mechanisms in EAD.

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