Journal
ORAL DISEASES
Volume 17, Issue 8, Pages 801-807Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1601-0825.2011.01839.x
Keywords
Sjogren's syndrome; innate immunity; sialoadenitis; mouse
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Funding
- National Institutes of Health, USA [R21DE019883, R01AI079621, R01DK069769]
- Sjogren's syndrome Foundation, USA
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OBJECTIVE: Sjogren's syndrome is a chronic autoimmune disorder characterized by progressive lymphocytic infiltration within the salivary and lacrimal glands. This study was undertaken to investigate the effects of innate immunity activation on sialoadenitis in a mouse strain genetically susceptible for development of SS-like disease. METHODS: Female New Zealand Black X New Zealand White F1 mice were repeatedly treated with toll-like 3 receptor agonist poly(I:C). Submandibular glands were investigated at different time points for sialoadenitis by immunohistochemistry and for gene expression of different chemokines by quantitative PCR. Submandibular gland-infiltrating cells were characterized by flow cytometry. RESULTS: Poly(I:C) treatment significantly upregulated the expression of multiple chemokines within the submandibular glands. The severity and incidence of sialoadenitis was considerably higher in poly(I:C)-treated mice. There was a preponderance of dendritic cells and NK cells in the initial inflammatory cell infiltrates, and these were followed by CD4+ T cells. CONCLUSIONS: Our data clearly demonstrate that systemic activation of innate immunity accelerates sialoadenitis in a mouse model for SS-like disease. These findings suggest that chronic activation of innate immunity can influence certain features of SS. Oral Diseases (2011) 17, 801-807
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