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原发性干燥综合征:唾液腺上皮细胞的新视角

Primary Sjögren's syndrome: new perspectives on salivary gland epithelial cells.

作者信息

Hou Jiaqi, Feng Yiyi, Yang Zhixia, Ding Yimei, Cheng Dandan, Shi Zhonghao, Li Rouxin, Xue Luan

机构信息

Rheumatology Department, Yueyang Hospital of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 110 Ganhe Road, Hongkou District, Shanghai, 200437, China.

Shanghai Skin Diseases Hospital, 200 Wuyi Road, Changning District, Shanghai, 200050, China.

出版信息

Eur J Med Res. 2024 Jul 17;29(1):371. doi: 10.1186/s40001-024-01967-5.

Abstract

Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease primarily affecting exocrine glands such as the salivary glands, leading to impaired secretion and sicca symptoms. As the mainstay of salivation, salivary gland epithelial cells (SGECs) have an important role in the pathology of pSS. Emerging evidence suggests that the interplay between immunological factors and SGECs may not be the initial trigger or the sole mechanism responsible for xerostomia in pSS, challenging conventional perceptions. To deepen our understanding, current research regarding SGECs in pSS was reviewed. Among the extensive aberrations in cellular architecture and function, this review highlighted certain alterations of SGECs that were identified to occur independently of or in absence of lymphocytic infiltration. In particular, some of these alterations may serve as upstream factors of immuno-inflammatory responses. These findings underscore the significance of introspecting the pathogenesis of pSS and developing interventions targeting SGECs in the early stages of the disease.

摘要

原发性干燥综合征(pSS)是一种主要影响唾液腺等外分泌腺的慢性自身免疫性疾病,导致分泌功能受损和口干症状。作为唾液分泌的主要承担者,唾液腺上皮细胞(SGECs)在pSS的病理过程中起重要作用。新出现的证据表明,免疫因素与SGECs之间的相互作用可能不是pSS口干症的初始触发因素或唯一机制,这对传统观念提出了挑战。为了加深我们的理解,本文对目前关于pSS中SGECs的研究进行了综述。在细胞结构和功能的广泛异常中,本综述强调了某些SGECs的改变,这些改变被确定为独立于淋巴细胞浸润或在无淋巴细胞浸润的情况下发生。特别是,其中一些改变可能作为免疫炎症反应的上游因素。这些发现强调了反思pSS发病机制以及在疾病早期开发针对SGECs的干预措施的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b8a/11253495/3d29d9e61281/40001_2024_1967_Fig1_HTML.jpg

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