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Abstract
Sjögren's syndrome (SS) is a complex rheumatoid disease that mainly affects exocrine glands, resulting in xerostomia (dry mouth) and xerophthalmia (dry eye). SS is characterized by autoantibodies, infiltration into exocrine glands, and ectopic expression of MHC II molecules on glandular epithelial cells. In contrast to the well-characterized clinical and immunological features, the etiology and pathogenesis of SS remain largely unknown. Animal models are powerful research tools for elucidating the pathogenesis of human diseases. To date, many mouse models of SS, including induced models, in which disease is induced in mice, and genetic models, in which mice spontaneously develop SS-like disease, have been established. These mouse models have provided new insight into the pathogenesis of SS. In this review, we aim to provide a comprehensive overview of recent advances in the field of experimental SS.
Highlights
Sjögren’s syndrome (SS) is a chronic autoimmune disorder characterized by oral and ocular dryness as a result of dysfunction [1]
Patients with SS are characterized by a broad clinical spectrum, including glandular and extraglandular manifestations as well as the development of B cell malignancy
Most mouse models for SS only develop a mild disease, and there is a lack of mouse models that show symptoms similar to primary SS (pSS) with systemic diseases with the exception of some mouse models for 2ndSS, such as Nonobese Diabetic (NOD) mice and BAFFtg mice, which develop multiple autoimmune disorders
Summary
Sjögren’s syndrome (SS) is a chronic autoimmune disorder characterized by oral and ocular dryness as a result of dysfunction [1]. In addition to the involvement of exocrine glands, extraglandular manifestations, such as inflammatory arthritis, purpura, Raynaud’s syndrome, interstitial lung disease, and renal disease, are observed in some patients with SS [6]. SS is characterized by the presence of autoantibodies, such as anti-SSA/Ro and anti-SSB/La, focal lymphocytic infiltrates in the exocrine glands, production of inflammatory cytokines, and ectopic expression of MHC II molecules on glandular epithelial cells [4, 7, 8]. Epidemiological, genetic, immunohistochemical, and in vitro studies with samples from SS patients and controls have shed light on the disease pathogenesis of SS [10,11,12]. Animal models, mice, provide us with a powerful tool to elucidate the development of human SS [13]
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