Activation of innate immunity accelerates sialoadenitis in a mouse model for Sjögren's syndrome-like disease

S. R. Nandula, Ym Scindia, P. Dey, H. Bagavant, Us Deshmukh

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

Sjögren'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.

Original languageEnglish (US)
Pages (from-to)801-807
Number of pages7
JournalOral Diseases
Volume17
Issue number8
DOIs
StatePublished - Nov 2011

Keywords

  • Innate immunity
  • Mouse
  • Sialoadenitis
  • Sjögren's syndrome

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