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Numerous models of exocrine tissue pathology related to autoimmune initiation of disease have been described, primarily by either immunohistology or histopathology. These model systems include inbred mouse strains that develop systemic lupus erythematosus, rheumatoid arthritis, graft vs. host disease, and diabetes. Commonly observed features of these mice include organized lymphocytic foci, composed of CD4+ and CD8+ T-cells, in both the salivary and the lacrimal glands. However, only the diabetic mouse model (NOD) undergoes a corresponding loss in exocrine gland function related to the presence of lymphocytic infiltrates. As we define the underlying pathophysiology of Sjögren's syndrome, the future of animal models for this disease will involve genetic exploration of candidate genes for development of autoimmune exocrinopathy.
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Michael G. Humphreys‐Beher (1996) studied this question.
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