唾液腺上皮细胞细胞因子在干燥综合征免疫病理学中的作用。

The role of cytokines from salivary gland epithelial cells in the immunopathology of Sjögren's syndrome.

机构信息

Department of Rheumatology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.

Department of Respiratory Disease, Thoracic Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

出版信息

Front Immunol. 2024 Sep 13;15:1443455. doi: 10.3389/fimmu.2024.1443455. eCollection 2024.

Abstract

In the pathogenesis and progression of Sjögren's syndrome (SS), hematopoietic cells in the peripheral circulation, tissue-resident immune cells, and parenchymal cells of salivary gland tissues (such as epithelial cells, endothelial cells, fibroblasts, etc.) all play crucial roles. These diverse cells form intricate networks and interact with each other, leading to tissue destruction and persistent chronic inflammation, ultimately causing irreversible damage in glandular function. Among these, salivary gland epithelial cells (SGECs) consistently hold a key position, characterized by their functions in expressing co-stimulatory and antigen-presenting molecules and secreting pro-inflammatory cytokines and chemokines. Moreover, SGECs actively engage in and facilitate the development of specific pathological structures within the salivary gland, such as lymphoepithelial lesions (LELs) and tertiary lymphoid structures (TLSs), thereby substantially elevating the risk of mucosa-associated lymphoid tissue (MALT) lymphoma. Overall, SGECs are recognized for their essential and irreplaceable contributions to the pathogenesis of SS. This review article initially delves into the anatomical composition of salivary gland epithelial cells, subsequently focusing on elucidating the different cytokines derived from SGECs, encompassing chemokines, pro-inflammatory cytokines, anti-inflammatory cytokines, pro-survival cytokines, and damage-associated molecular patterns (DAMPs), to explore their key roles in the pathogenesis of SS.

摘要

在干燥综合征(SS)的发病机制和进展中,外周循环中的造血细胞、组织固有免疫细胞和唾液腺组织的实质细胞(如上皮细胞、内皮细胞、成纤维细胞等)都起着至关重要的作用。这些不同的细胞形成复杂的网络并相互作用,导致组织破坏和持续的慢性炎症,最终导致腺体功能的不可逆转损伤。在这些细胞中,唾液腺上皮细胞(SGECs)一直处于关键地位,其特征是表达共刺激和抗原呈递分子以及分泌促炎细胞因子和趋化因子。此外,SGECs 还积极参与并促进唾液腺内特定病理结构的发展,如淋巴上皮病变(LELs)和三级淋巴样结构(TLSs),从而大大增加了黏膜相关淋巴组织(MALT)淋巴瘤的风险。总的来说,SGECs 被认为对 SS 的发病机制具有重要且不可替代的作用。这篇综述文章首先探讨了唾液腺上皮细胞的解剖组成,随后重点阐述了源自 SGECs 的不同细胞因子,包括趋化因子、促炎细胞因子、抗炎细胞因子、促生存细胞因子和损伤相关分子模式(DAMPs),以探讨它们在 SS 发病机制中的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f687/11427401/31528c942dd4/fimmu-15-1443455-g001.jpg

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