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Douglas A. Jabs, Bella Lee, Judith Whittum-Hudson, Robert A. Prendergast; The Role of Fas-Fas Ligand–Mediated Apoptosis in Autoimmune Lacrimal Gland Disease in MRL/MpJ Mice. Invest. Ophthalmol. Vis. Sci. 2001;42(2):399-401.
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purpose. MRL/MpJ mice spontaneously develop lacrimal gland inflammation and are a model
for the human disorder Sjögren’s syndrome. MRL/MpJ-lpr/lpr
(MRL/lpr) and MRL/Mp-+/+ (MRL/+) mice are congenic substrains, which
differ only by a single autosomal recessive gene, the lpr mutation. This mutation results in defective Fas protein, defective
lymphocytic apoptosis, and accelerated autoimmune lacrimal gland
disease in MRL/lpr mice. We evaluated apoptosis in the lacrimal glands
of MRL/lpr and MRL/+ mice.
methods. Inflammatory cells in the lacrimal glands of MRL/lpr and MRL/+ mice
were evaluated for apoptosis with TUNEL staining and Fas and Fas ligand
expression with immunohistochemistry.
results. MRL/lpr mice had a greater percentage of the lacrimal gland replaced by
inflammatory infiltrate (30.3% ± 7.0%) than did MRL/+ mice (13.0%±
3.0%, P = 0.02). However, similar amounts of
lymphocytic apoptosis were present in the lacrimal glands of MRL/lpr
and MRL/+ mice. The mean number of apoptotic cells per unit area of
inflammation was 23.8 ± 2.4 in MRL/lpr mice and 24.6 ± 6.0
in MRL/+ mice (P = 0.91). Fas expression was absent on
lymphocytes in MRL/lpr mice but was present on lymphocytes in MRL/+
mice. Fas ligand expression was present on epithelial structures in
conclusions. The accelerated lacrimal gland disease inflammation in MRL/lpr mice
does not appear to be due to decreased apoptosis in the
microenvironment of the lacrimal gland of MRL/lpr mice. It appears that
in MRL/lpr mice there is defective extrathymic lymphoid apoptosis,
permitting a relatively greater expansion of autoreactive T cells,
which subsequently invade the lacrimal gland.
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