Abstract
Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by severe inflammation of exocrine glands such as the salivary and lacrimal glands. When it affects the lacrimal glands, many patients experience keratoconjunctivitis due to severely dry eyes. This study investigated the pathological and immunological characteristics of ocular lesions in a mouse model of SS. Corneal epithelial injury and hyperplasia were confirmed pathologically. The number of conjunctival mucin-producing goblet cells was significantly decreased in the SS model mice compared with control mice. Expression levels of transforming growth factor (TGF)-β, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and C-X-C motif chemokine (CXCL) 12 were significantly higher in the corneal epithelium of the SS model mice than in control mice. Inflammatory lesions were observed in the Harderian, intraorbital, and extraorbital lacrimal glands in the SS model mice, suggesting that the ocular glands were targeted by an autoimmune response. The lacrimal glands of the SS model mice were infiltrated by cluster of differentiation (CD)4+ T cells. Real-time reverse transcription-polymerase chain reaction (RT-PCR) revealed significantly increased mRNA expression of TNF-α, TGF-β, CXCL9, and lysozyme in the extraorbital lacrimal glands of the SS model mice compared with control mice. These results add to the understanding of the complex pathogenesis of SS and may facilitate development of new therapeutic strategies.
Highlights
Sjögren’s syndrome (SS) is an autoimmune disease affecting the exocrine glands, including the lacrimal and salivary glands, causing dry eyes and mouth symptoms such as severe keratoconjunctivitis and oral disorders [1]
The pathogenesis and molecular mechanisms of SS have been investigated in various animal models of SS [5], including a thymectomized neonatal NFS/sublingual gland mutant mouse model, which we developed to study SS and the therapeutic effects of several reagents on its autoimmune lesions [6,7,8,9,10]
Lesions of the cornea and lacrimal glands produced in the mouse model were evaluIantetdhispastthuodlyo,gliecsailolynsaonfdthoecucolarrnelaesaionnds lawcreirme aelvgallaunadtesdpriomdmucuendoliongtihcaellmy otuosebrmoaoddeenl woeurre uenvdaelursattaenddipnagthoof ltohgeicpaaltlhyogaenndesoiscuolfaSrSlaeusitoonims mwuenreitye.valuated immunologically to broaden our understanding of the pathogenesis of SS autoimmunity
Summary
Sjögren’s syndrome (SS) is an autoimmune disease affecting the exocrine glands, including the lacrimal and salivary glands, causing dry eyes and mouth symptoms such as severe keratoconjunctivitis and oral disorders [1]. The pathogenesis and molecular mechanisms of SS have been investigated in various animal models of SS [5], including a thymectomized neonatal NFS/sublingual gland (sld) mutant mouse model, which we developed to study SS and the therapeutic effects of several reagents on its autoimmune lesions [6,7,8,9,10]. The detailed ocular lesions in the eyeball, cornea, iris, and lacrimal gland lesions in the mouse models are not fully understood due to the complicated anatomy and small structures. Lesions of the cornea and lacrimal glands produced in the mouse model were evaluIantetdhispastthuodlyo,gliecsailolynsaonfdthoecucolarrnelaesaionnds lawcreirme aelvgallaunadtesdpriomdmucuendoliongtihcaellmy otuosebrmoaoddeenl woeurre uenvdaelursattaenddipnagthoof ltohgeicpaaltlhyogaenndesoiscuolfaSrSlaeusitoonims mwuenreitye.valuated immunologically to broaden our understanding of the pathogenesis of SS autoimmunity
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