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T 细胞转录因子（T-bet）B 细胞在肥胖期间在脂肪组织中积累，并加剧代谢紊乱。

T-bet B cells accumulate in adipose tissue and exacerbate metabolic disorder during obesity.

机构信息

Department of Microbiology, Immunology & Molecular Genetics, UT Health, San Antonio, TX 78229, USA.

Department of Microbiology, Immunology & Molecular Genetics, UT Health, San Antonio, TX 78229, USA.

出版信息

Cell Metab. 2022 Aug 2;34(8):1121-1136.e6. doi: 10.1016/j.cmet.2022.07.002. Epub 2022 Jul 21.

DOI:10.1016/j.cmet.2022.07.002
PMID:35868310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9357106/
Abstract

Obesity is accompanied by inflammation in adipose tissue, impaired glucose tolerance, and changes in adipose leukocyte populations. These studies of adipose tissue from humans and mice revealed that increased frequencies of T-bet B cells in adipose tissue depend on invariant NKT cells and correlate with weight gain during obesity. Transfer of B cells enriched for T-bet cells exacerbates metabolic disorder in obesity, while ablation of Tbx21 specifically in B cells reduces serum IgG2c levels, inflammatory cytokines, and inflammatory macrophages in adipose tissue, ameliorating metabolic symptoms. Furthermore, transfer of serum or purified IgG from HFD mice restores metabolic disease in T-bet B cell-deficient mice, confirming T-bet B cell-derived IgG as a key mediator of inflammation during obesity. Together, these findings reveal an important pathological role for T-bet B cells that should inform future immunotherapy design in type 2 diabetes and other inflammatory conditions.

摘要

肥胖伴随着脂肪组织炎症、葡萄糖耐量受损和脂肪白细胞群体的变化。这些来自人类和小鼠脂肪组织的研究表明，脂肪组织中 T-bet B 细胞的频率增加取决于不变自然杀伤 T 细胞，并与肥胖期间的体重增加相关。富含 T-bet 细胞的 B 细胞的转移会加剧肥胖中的代谢紊乱，而 Tbx21 特异性在 B 细胞中的缺失会降低血清 IgG2c 水平、炎症细胞因子和脂肪组织中的炎症巨噬细胞，改善代谢症状。此外，从高脂肪饮食小鼠中转移血清或纯化 IgG 可恢复 T-bet B 细胞缺陷小鼠的代谢疾病，证实 T-bet B 细胞衍生的 IgG 是肥胖期间炎症的关键介质。总之，这些发现揭示了 T-bet B 细胞的重要病理作用，这将为 2 型糖尿病和其他炎症性疾病的未来免疫治疗设计提供信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ce9/9357106/dd73cc67907b/nihms-1823411-f0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ce9/9357106/dd73cc67907b/nihms-1823411-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ce9/9357106/468e36f917da/nihms-1823411-f0001.jpg
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1
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2
Immunology of Aging: the Birth of Inflammaging.衰老免疫学：炎症衰老的诞生。
Clin Rev Allergy Immunol. 2023 Apr;64(2):109-122. doi: 10.1007/s12016-021-08899-6. Epub 2021 Sep 18.
3
Phenotypic and Functional Characterization of Double Negative B Cells in the Blood of Individuals With Obesity.肥胖个体血液中双阴性 B 细胞的表型和功能特征。
B细胞衍生的孤啡肽/孤啡肽FQ导致肥胖症患者葡萄糖耐量受损和胰岛素抵抗。
iScience. 2025 Jun 4;28(7):112819. doi: 10.1016/j.isci.2025.112819. eCollection 2025 Jul 18.
4
T-bet-expressing B cells promote atherosclerosis in apolipoprotein E-deficient mice.表达T-bet的B细胞促进载脂蛋白E缺陷小鼠的动脉粥样硬化。
J Immunol. 2025 Feb 26;214(3):317-24. doi: 10.1093/jimmun/vkae027.
5
Can invariant Natural Killer T cells drive B cell fate? a look at the humoral response.不变自然杀伤T细胞能驱动B细胞命运吗？审视体液免疫反应。
Front Immunol. 2025 Feb 18;16:1505883. doi: 10.3389/fimmu.2025.1505883. eCollection 2025.
6
Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.自身免疫性疾病中与年龄相关的B细胞：发病机制及临床意义
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7
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J Ovarian Res. 2025 Feb 5;18(1):23. doi: 10.1186/s13048-025-01606-5.
8
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9
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Front Immunol. 2021 Feb 23;12:616650. doi: 10.3389/fimmu.2021.616650. eCollection 2021.
4
Distinct iNKT Cell Populations Use IFNγ or ER Stress-Induced IL-10 to Control Adipose Tissue Homeostasis.不同的 iNKT 细胞群体利用 IFNγ 或 ER 应激诱导的 IL-10 来控制脂肪组织稳态。
Cell Metab. 2020 Aug 4;32(2):243-258.e6. doi: 10.1016/j.cmet.2020.05.017. Epub 2020 Jun 8.
5
Age-Associated B Cells.与年龄相关的 B 细胞。
Annu Rev Immunol. 2020 Apr 26;38:315-340. doi: 10.1146/annurev-immunol-092419-031130. Epub 2020 Jan 27.
6
Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis.衰老诱导脂肪细胞中依赖 Nlrp3 炎性小体的扩增，从而损害代谢稳态。
Cell Metab. 2019 Dec 3;30(6):1024-1039.e6. doi: 10.1016/j.cmet.2019.10.006. Epub 2019 Nov 14.
7
Lupus Autoimmunity and Metabolic Parameters Are Exacerbated Upon High Fat Diet-Induced Obesity Due to TLR7 Signaling.狼疮自身免疫和代谢参数因 TLR7 信号导致高脂肪饮食诱导的肥胖而加重。
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Cell Rep. 2018 Jul 24;24(4):824-837.e3. doi: 10.1016/j.celrep.2018.06.074.
9
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Nat Commun. 2018 May 1;9(1):1758. doi: 10.1038/s41467-018-03750-7.
10
Regulation of age-associated B cells by IRF5 in systemic autoimmunity.IRF5 调节系统性自身免疫中的与年龄相关的 B 细胞。
Nat Immunol. 2018 Apr;19(4):407-419. doi: 10.1038/s41590-018-0056-8. Epub 2018 Feb 26.