title: Activation of innate immunity accelerates sialoadenitis in a mouse model for Sjögren's syndrome-like disease.
abstract: OBJECTIVE
  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.
authors.affiliation: Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA.
authors.forename: S-R
authors.initials: SR
authors.lastname: Nandula
authors.forename: Y M
authors.initials: YM
authors.lastname: Scindia
authors.forename: P
authors.initials: P
authors.lastname: Dey
authors.forename: H
authors.initials: H
authors.lastname: Bagavant
authors.forename: U S
authors.initials: US
authors.lastname: Deshmukh
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000473:pathology; D054413:Chemokine CCL11 / Q000032:analysis / Q000187:drug effects; D018932:Chemokine CCL2 / Q000032:analysis / Q000187:drug effects; D054405:Chemokine CCL3 / Q000032:analysis / Q000187:drug effects; D054407:Chemokine CCL4 / Q000032:analysis / Q000187:drug effects; D054410:Chemokine CCL7 / Q000032:analysis / Q000187:drug effects; D054357:Chemokine CXCL10 / Q000032:analysis / Q000187:drug effects; D054382:Chemokine CXCL13 / Q000032:analysis / Q000187:drug effects; D019742:Chemokines, CC / Q000032:analysis / Q000187:drug effects; D019743:Chemokines, CXC / Q000032:analysis / Q000187:drug effects; D003713:Dendritic Cells / Q000187:drug effects / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology*; D007694:Killer Cells, Natural / Q000187:drug effects / Q000473:pathology; D051379:Mice; D008814:Mice, Inbred NZB; D018945:Monocyte Chemoattractant Proteins / Q000032:analysis / Q000187:drug effects; D011070:Poly I-C / Q000494:pharmacology; D060888:Real-Time Polymerase Chain Reaction; D012793:Sialadenitis / Q000276:immunology* / Q000473:pathology; D012859:Sjogren's Syndrome / Q000276:immunology* / Q000473:pathology; D013364:Submandibular Gland Diseases / Q000276:immunology / Q000473:pathology; D051196:Toll-Like Receptor 3 / Q000819:agonists
chemical_list: C515457:Ccl11 protein, mouse; C491224:Ccl12 protein, mouse; C491768:Ccl2 protein, mouse; C496534:Ccl3 protein, mouse; C515451:Ccl7 protein, mouse; D054413:Chemokine CCL11; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054410:Chemokine CCL7; D054357:Chemokine CXCL10; D054382:Chemokine CXCL13; D019742:Chemokines, CC; D019743:Chemokines, CXC; C485433:Cxcl10 protein, mouse; C486386:Cxcl13 protein, mouse; D018945:Monocyte Chemoattractant Proteins; C519703:TLR3 protein, mouse; D051196:Toll-Like Receptor 3; D011070:Poly I-C