title: Mechanism of the development of autoimmune dacryodenitis in the mouse model for primary Sjögren's syndrome.
abstract: To elucidate the mechanism of development in autoimmune lacrimal gland disease, we analyzed different aspects of autoimmune dacryoadenitis in a newly established mouse model for primary Sjögren's syndrome, focusing on the local expressions of cytokine genes, and the repertoire of T cell receptor (TCR) V beta genes transcribed within the inflammatory infiltration in the lacrimal glands. We found that the vast majority of inflammatory infiltration into the lacrimal glands were CD4+ V beta 8+ T cells. We detected the up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-10, IL-12p40) in the lacrimal glands with very early inflammatory lesions by reverse transcriptase (RT)-PCR analysis. The predominant expression of the V beta 8 gene segment was detected from a very early stage, while extensive age-related diversity of TCR V beta gene usage was observed. Single-strand conformation polymorphism (SSCP) analysis demonstrated a distinct and a common binding pattern in the PCR product of the V beta 8 gene on the infiltrating cells during the course of the disease. These data suggest that in autoimmune dacryoadenitis of the mouse model for primary Sjögren's syndrome there may be a restricted usage of TCR V beta elements on a very early stage of the autoimmune lesion to recognize unknown self-antigen, and the autoreactive CD4+ T cells constitute a unique cytokine profile in the autoimmune lacrimal gland disease.
authors.affiliation: Department of Ophthalmology, School of Medicine, University of Tokushima, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Mimura
authors.forename: H
authors.initials: H
authors.lastname: Hamano
authors.forename: N
authors.initials: N
authors.lastname: Haneji
authors.forename: K
authors.initials: K
authors.lastname: Yanagi
authors.forename: Y
authors.initials: Y
authors.lastname: Hayashi
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D001483:Base Sequence; D016207:Cytokines / Q000235:genetics; D003607:Dacryocystitis / Q000209:etiology* / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression / Q000276:immunology; D007150:Immunohistochemistry; D051379:Mice; D008815:Mice, Inbred Strains; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics; D012859:Sjogren's Syndrome / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D016207:Cytokines; D016693:Receptors, Antigen, T-Cell, alpha-beta