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REVIEW article
Front. Immunol.
Sec. B Cell Biology
Volume 15 - 2024 |
doi: 10.3389/fimmu.2024.1450366
The role of B cells in the pathogenesis of type 1 diabetes
Provisionally accepted- 1 Yangtze University, Jingzhou, China
- 2 Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
- 3 The First Affiliated Hospital of Yangtze University, Jingzhou, Hubei Province, China
Type 1 diabetes (T1D) is a metabolic disorder caused by a complete lack of insulin, primarily manifested by hyperglycemia. The mechanisms underlying the onset of T1D are complex, involving genetics, environment, and various unknown factors, leading to the infiltration of various immune components into the islets. Besides T cells, B cells are now considered important contributors to the pathogenesis of T1D, according to recent studies. In Non-Obese Diabetic(NOD) mice, the absence of B cells prevents the development of T1D, and B cell depletion can even restore the function of pancreatic β -cells, emphasizing their involvement in the development of T1D. Naturally, besides pathogenic B cells, regulatory B cells (Bregs) might have a protective function in T1D. This article examines the mechanisms behind B cell tolerance and the defects in B cell tolerance checkpoints in T1D.We explored possible functions of B cells in T1D, including the role of islet autoantibodies in T1D, TB cell interactions, and the role of Bregs in the pathogenesis of T1D. We also summarized the advances of B cell-targeted therapy, exploring new methods for intervention and treatment of T1D.
Keywords: type 1 diabetes, B cells, T cells, regulatory B cells, Marginal
Received: 18 Jun 2024; Accepted: 29 Nov 2024.
Copyright: © 2024 Zheng, Gong, Zhong, Wang, Li, Huang, Chen, Nie, LIU and Zou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Bing Zheng, Yangtze University, Jingzhou, China
Quan Gong, Yangtze University, Jingzhou, China
Jixin Zhong, Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China
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