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糖尿病关联:1型糖尿病中胰岛免疫细胞界面的B细胞

Dia-B-Ties: B Cells in the Islet-Immune-Cell Interface in T1D.

作者信息

Hilliard Brandon K, Prendergast Jessica E, Smith Mia J

机构信息

Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO 80045, USA.

Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

出版信息

Biomolecules. 2025 Feb 25;15(3):332. doi: 10.3390/biom15030332.

DOI:10.3390/biom15030332
PMID:40149868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11940010/
Abstract

Type 1 diabetes (T1D) is an autoimmune disease that affects an estimated 30 million people worldwide and results in a lifelong dependency of exogenous insulin treatments. While T1D is characterized by T-cell driven-destruction of the insulin-secreting β cells, B lymphocytes play a key role in the islet-immune interface. B cells are an essential intermediary between islet cells and other immune-cell populations. Through antigen presentation, cytokine secretion, and antibody production, B cells play a role in activating autoreactive islet-specific T cells, thus potentiating pancreatic inflammation in the early stages of T1D. Despite this, their role in disease development remains an understudied feature of T1D with significant therapeutic potential. Herein, we will discuss the current knowledge of the islet-immune-cell interface within T1D through the lens of B lymphocytes. We will also consider knowledge gaps that may be limiting further therapeutic opportunities.

摘要

1型糖尿病(T1D)是一种自身免疫性疾病,全球约有3000万人受其影响,患者终生依赖外源性胰岛素治疗。虽然T1D的特征是T细胞驱动胰岛素分泌β细胞的破坏,但B淋巴细胞在胰岛免疫界面中起关键作用。B细胞是胰岛细胞与其他免疫细胞群体之间的重要中介。通过抗原呈递、细胞因子分泌和抗体产生,B细胞在激活自身反应性胰岛特异性T细胞中发挥作用,从而在T1D早期加剧胰腺炎症。尽管如此,它们在疾病发展中的作用仍是T1D中一个研究不足但具有巨大治疗潜力的特征。在此,我们将通过B淋巴细胞的视角讨论目前关于T1D中胰岛免疫细胞界面的知识。我们还将考虑可能限制进一步治疗机会的知识空白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/abe34429906f/biomolecules-15-00332-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/a75315a5ca58/biomolecules-15-00332-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/6321aee87717/biomolecules-15-00332-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/94da81163af5/biomolecules-15-00332-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/abe34429906f/biomolecules-15-00332-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/a75315a5ca58/biomolecules-15-00332-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/6321aee87717/biomolecules-15-00332-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/94da81163af5/biomolecules-15-00332-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ca/11940010/abe34429906f/biomolecules-15-00332-g004.jpg

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本文引用的文献

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TNF-α inhibitors for type 1 diabetes: exploring the path to a pivotal clinical trial.TNF-α 抑制剂治疗 1 型糖尿病:探索关键临床试验之路。
Front Immunol. 2024 Oct 1;15:1470677. doi: 10.3389/fimmu.2024.1470677. eCollection 2024.
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The Role of B Lymphocytes in Type 1 Diabetes.B淋巴细胞在1型糖尿病中的作用。
Cold Spring Harb Perspect Med. 2024 Aug 12. doi: 10.1101/cshperspect.a041593.
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Selective CAR T cell-mediated B cell depletion suppresses IFN signature in SLE.选择性 CAR T 细胞介导的 B 细胞耗竭可抑制 SLE 中的 IFN 特征。
JCI Insight. 2024 May 9;9(12):e179433. doi: 10.1172/jci.insight.179433.
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An antigen-specific immunotherapeutic, AKS-107, deletes insulin-specific B cells and prevents murine autoimmune diabetes.一种抗原特异性免疫疗法,AKS-107,可删除胰岛素特异性 B 细胞并预防小鼠自身免疫性糖尿病。
Front Immunol. 2024 Mar 7;15:1367514. doi: 10.3389/fimmu.2024.1367514. eCollection 2024.
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Tertiary lymphoid structures and B cells determine clinically relevant T cell phenotypes in ovarian cancer.三级淋巴结构和 B 细胞决定卵巢癌中具有临床相关性的 T 细胞表型。
Nat Commun. 2024 Mar 21;15(1):2528. doi: 10.1038/s41467-024-46873-w.
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An immune cell map of human lung adenocarcinoma development reveals an anti-tumoral role of the Tfh-dependent tertiary lymphoid structure.人类肺腺癌发展的免疫细胞图谱揭示了 Tfh 依赖性三级淋巴结构的抗肿瘤作用。
Cell Rep Med. 2024 Mar 19;5(3):101448. doi: 10.1016/j.xcrm.2024.101448. Epub 2024 Mar 8.
7
An Insulin-Chromogranin A Hybrid Peptide Activates DR11-Restricted T Cells in Human Type 1 Diabetes.胰岛素-嗜铬粒蛋白 A 杂合肽在人类 1 型糖尿病中激活 DR11 限制性 T 细胞。
Diabetes. 2024 May 1;73(5):743-750. doi: 10.2337/db23-0622.
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Diagnostics (Basel). 2023 Sep 4;13(17):2859. doi: 10.3390/diagnostics13172859.
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Inflammation versus regulation: how interferon-gamma contributes to type 1 diabetes pathogenesis.炎症与调节:干扰素-γ如何促成1型糖尿病的发病机制
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