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From the Departments of Pathology,*
Laboratory
Medicine,
and
Orthodontics,
Tokushima University School of
Dentistry, Tokushima, Japan
When we evaluated the age-associated changes in autoimmune
exocrinopathy in a NFS/sld murine model for primary
Sjögrens syndrome (SS), severe destructive autoimmune
lesions developed in the salivary and lacrimal glands in the aged
mice, compared with those observed in the younger model. We
detected a decreased secretion of saliva and tear flow in the aged
group. A significant increase of TUNEL+-apoptotic
epithelial duct cells in the salivary glands was detected in the aged
SS animal model. A higher proportion of mouse salivary gland cells
bearing Fas was found in the aged group, whereas no
significant changes were seen on tissue-infiltrating CD4+ T
cells bearing FasL in the salivary glands from young and aged mice. We
detected an increased cleavage product of organ-specific
autoantigen, 120-kd
-fodrin, in the aged salivary
gland tissues on immunoblotting, and an increase in serum
autoantibody production against 120-kd
-fodrin by enzyme-linked
immunosorbent assay. An increase in the proliferative response of
splenic T cells against organ-specific autoantigen was
observed, whereas nonspecific concanavalin A
responsiveness was decreased in the aged mice. In addition, a
decrease in Fas expression was found on splenic CD4+ T
cells in the aged mice, and anti-Fas mAb-stimulated apoptosis
was down-regulated on CD4+ T cells. These results
indicate that age-associated dysregulation of CD4+ T cells
may play a crucial role on acceleration of organ-specific autoimmune
lesions in a murine model for primary SS through Fas-mediated
apoptosis.
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