title: Experimental autoallergic sialadenitis in the LEW rat. I. Parameters of disease induction.
abstract: Experimental autoallergic sialadenitis (EAS) is an autoimmune mononuclear cell infiltration of the submandibular salivary gland that results in tissue destruction and glandular dysfunction. A previous report has described an animal model of induced EAS in LEW rats following sensitization with allogeneic WF submandibular gland (SMG). The present study extends this observation to an EAS disease model induced following sensitization of LEW rats with syngeneic LEW SMG. Furthermore, we describe the characterization of the mononuclear cells in the glandular infiltrates, evaluate the production of autoantibodies, and establish the parameters important for reproducible induction of EAS. Our results demonstrate that EAS can be induced in a completely syngeneic system and the histopathology of disease induction in the syngeneic and allogeneic model systems is similar. Helper/inducer (CD4+) and suppressor/cytotoxic (CD8+) T-cell subsets are the dominant cell types in the salivary mononuclear cell infiltrate. An anti-duct autoantibody was found in the serum of virtually all LEW rats with EAS. Although closely associated with disease development, the presence of this antibody was not a prerequisite for development of histopathologic disease. Induction of disease in both the syngeneic and allogeneic models of EAS is dependent upon administration of Bordetella pertussis at the time of sensitization. Finally, the histopathology of the cellular infiltrates in both the allogeneic and syngeneic models of EAS resemble those observed in the salivary tissues of Sjögren's patients. While there are several differences between EAS in the LEW rat and the full expression of Sjögren's syndrome, EAS may serve as a model to study the salivary gland component of this complex human disease.
authors.affiliation: Department of Oral Diagnosis, School of Dental Medicine, University of Connecticut Health Center, Farmington 06030.
authors.forename: L S
authors.initials: LS
authors.lastname: Cutler
authors.forename: D
authors.initials: D
authors.lastname: Rozenski
authors.forename: J
authors.initials: J
authors.lastname: Coolens
authors.forename: J
authors.initials: J
authors.lastname: Rozing
authors.forename: M
authors.initials: M
authors.lastname: Angelillo
authors.forename: A L
authors.initials: AL
authors.lastname: Wayne
authors.forename: K M
authors.initials: KM
authors.lastname: Fitzgerald
authors.forename: D L
authors.initials: DL
authors.lastname: Greiner
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D001323:Autoantibodies / Q000096:biosynthesis; D001327:Autoimmune Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D010641:Phenotype; D051381:Rats; D011917:Rats, Inbred Lew; D012793:Sialadenitis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D013363:Submandibular Gland / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D001323:Autoantibodies