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B cells promote inflammation in obesity and type 2 diabetes through regulation of T-cell function and an inflammatory cytokine profile
Open accessAbstract
Patients with type 2 diabetes (T2D) have disease-associated changes in B-cell function, but the role these changes play in disease pathogenesis is not well established. Data herein show B cells from obese mice produce a proinflammatory cytokine profile compared with B cells from lean mice. Complementary in vivo studies show that obese B cell–null mice have decreased systemic inflammation, inflammatory B- and T-cell cytokines, adipose tissue inflammation, and insulin resistance (IR) compared with obese WT mice. Reduced inflammation in obese/insulin resistant B cell–null mice associates with an increased percentage of anti-inflammatory regulatory T cells (Tregs). This increase contrasts with the sharply decreased percentage of Tregs in obese compared with lean WT mice and suggests that B cells may be critical regulators of T-cell functions previously shown to play important roles in IR. We demonstrate that B cells from T2D (but not non-T2D) subjects support proinflammatory T-cell function in obesity/T2D through contact-dependent mechanisms. In contrast, human monocytes increase proinflammatory T-cell cytokines in both T2D and non-T2D analyses. These data support the conclusion that B cells are critical regulators of inflammation in T2D due to their direct ability to promote proinflammatory T-cell function and secrete a proinflammatory cytokine profile. Thus, B cells are potential therapeutic targets for T2D.
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“Adipose tissue‐resident B cells, which are localized around macrophage clusters, have also been shown to have a predominant pathogenic role in obesity‐related IR in mice.[ 68 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [68]
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“These pathogenic B cells activate IFNγ‐producing CD4+ and CD8 + T cells and/or IL‐17‐secreting Th1 cells within the visceral adipose tissues, presumably through LTB4/leukotriene‐B4 receptor 1 (LTB4R1) signalling.”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [68]
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Metadata
- Authors
- DeFuria, J., Belkina, A. C., Jagannathan-Bogdan, M., Snyder-Cappione, J., Carr, J. D., Nersesova, Y. R., Markham, D., Strissel, K. J., Watkins, A. A., Zhu, M., Allen, J., Bouchard, J., Toraldo, G., Jasuja, R., Obin, M. S., McDonnell, M. E., Apovian, C., Denis, G. V., & Nikolajczyk, B. S.
- Affiliations
- Boston University (US)
- Cancer Research Center (US)
- Department of Pathology, Boston University School of Medicine, Boston, MA 02118;
- Department of Microbiology,
- Boston Medical Center (US)
- Tufts University (US)
- Renal Section and
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2013-03-11
- Volume
- 110
- Issue
- 13
- Pages
- 5133-5138
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3612635
- OpenAlex
- W2144821774
- Cited by
- 521
- References
- 39
- Citations by year
- 2026: 17 · 2025: 36 · 2024: 31 · 2023: 32 · 2022: 50 · 2021: 50 · 2020: 43 · 2019: 37 · 2018: 42 · 2017: 51 · 2016: 36 · 2015: 41 · 2014: 31 · 2013: 23
- FWCI
- 32.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Boston Area Diabetes Endocrinology Research Center (DK046200)
- National Institutes of Health (DK046200, AI007309)
- Boston Nutrition Obesity Research Center, Boston University
- National Heart, Lung, and Blood Institute (T32HL007501, HL007501)
- National Cancer Institute (U01CA182898)
- National Institute of Allergy and Infectious Diseases (T32AI007309, AI007309)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK090455, P30DK046200, DK046200, R21DK089270, R56DK096525)
- National Institute of Dental and Craniofacial Research (R21DE021154)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- B cells, type 2 diabetes, obesity, inflammation, insulin resistance, regulatory T cells, T cell function, inflammatory cytokines, adipose tissue inflammation, monocytes, contact-dependent signaling, therapeutic target
- MeSH terms
- Animals, B-Lymphocytes, Diabetes Mellitus, Type 2, Female, Humans, Inflammation, Male, Mice, Obese, Obesity, Cytokines, T-Lymphocytes, Regulatory, Mice
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