Science and Mathematics Faculty Publications

Loss of PKCδ results in characteristics of Sjögren’s syndrome including salivary gland dysfunction

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Oral Diseases





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Chronic infiltration of lymphocytes into the salivary and lacrimal glands of Sjögren’s Syndrome patients leads to destruction of acinar cells and loss of exocrine function. Protein kinase C-delta (PKCδ) is known to play a critical role in B cell maintenance. Mice in which the PKCδ gene has been disrupted have a loss of B cell tolerance, multiple organ lymphocytic infiltration, and altered apoptosis. To determine if PKCδ contributes to the pathogenesis of Sjögren’s Syndrome, we quantified changes in indicators of Sjögren’s Syndrome in PKCδ−/− mice as a function of age. Salivary gland histology, function, the presence of autoantibodies, and cytokine expression were examined. Materials and Methods: Submandibular glands were examined for the presence of lymphocytic infiltrates, and the type of infiltrating lymphocyte and cytokine deposition was evaluated by immunohistochemistry. Serum samples were tested by autoantibody screening, which was graded by its staining pattern and intensity. Salivary gland function was determined by saliva collection at various ages. Results: PKCδ−/− mice have reduced salivary gland function, B220+ B cell infiltration, anti-nuclear antibody production, and elevated IFN-γ in the salivary glands as compared to PKCδ+/+ littermates. Conclusions: PKCδ−/− mice have exocrine gland tissue damage indicative of a Sjögren’s Syndrome-like phenotype.


Autoimmunity, Sjögren’s syndrome