| Cell & Bioscience | |
| Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes | |
| Review | |
| Tian-Tian Yue1  Fa-Xi Wang2  Wan-Ying Lu2  Jia-Hui Luo2  Chun-Liang Yang2  Shan-Jie Rong2  Shi-Wei Liu3  Fei Sun4  Cong-Yi Wang4  | |
| [1] Devision of Nutrition, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;NHC Key Laboratory of Respiratory Diseases, Department of Respiratory and Critical Care Medicine, The Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China;Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China;NHC Key Laboratory of Respiratory Diseases, Department of Respiratory and Critical Care Medicine, The Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; | |
| 关键词: Type 1 diabetes (T1D); Pancreatic draining lymph nodes (PLNs); Signal inputs; PLN remodeling; Signal outputs; | |
| DOI : 10.1186/s13578-023-01110-7 | |
| received in 2023-03-08, accepted in 2023-08-21, 发布年份 2023 | |
| 来源: Springer | |
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【 摘 要 】
Type 1 diabetes (T1D) is a chronic, progressive autoinflammatory disorder resulting from the breakdown of self-tolerance and unrestrained β cell-reactive immune response. Activation of immune cells is initiated in islet and amplified in lymphoid tissues, especially those pancreatic draining lymph nodes (PLNs). The knowledge of PLNs as the hub of aberrant immune response is continuously being replenished and renewed. Here we provide a PLN-centered view of T1D pathogenesis and emphasize that PLNs integrate signal inputs from the pancreas, gut, viral infection or peripheral circulation, undergo immune remodeling within the local microenvironment and export effector cell components into pancreas to affect T1D progression. In accordance, we suggest that T1D intervention can be implemented by three major ways: cutting off the signal inputs into PLNs (reduce inflammatory β cell damage, enhance gut integrity and control pathogenic viral infections), modulating the immune activation status of PLNs and blocking the outputs of PLNs towards pancreatic islets. Given the dynamic and complex nature of T1D etiology, the corresponding intervention strategy is thus required to be comprehensive to ensure optimal therapeutic efficacy.
【 授权许可】
CC BY
© Society of Chinese Bioscientists in America (SCBA) 2023
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO202309156167415ZK.pdf | 1407KB | ||
| 40517_2023_266_Article_IEq6.gif | 1KB | Image | |
| 40854_2023_507_Article_IEq23.gif | 1KB | Image | |
| Fig. 2 | 79KB | Image |
【 图 表 】
Fig. 2
40854_2023_507_Article_IEq23.gif
40517_2023_266_Article_IEq6.gif
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