B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies
Open accessAbstract
Chronic inflammation characterized by T cell and macrophage infiltration of visceral adipose tissue (VAT) is a hallmark of obesity-associated insulin resistance and glucose intolerance. Here we show a fundamental pathogenic role for B cells in the development of these metabolic abnormalities. B cells accumulate in VAT in diet-induced obese (DIO) mice, and DIO mice lacking B cells are protected from disease despite weight gain. B cell effects on glucose metabolism are mechanistically linked to the activation of proinflammatory macrophages and T cells and to the production of pathogenic IgG antibodies. Treatment with a B cell-depleting CD20 antibody attenuates disease, whereas transfer of IgG from DIO mice rapidly induces insulin resistance and glucose intolerance. Moreover, insulin resistance in obese humans is associated with a unique profile of IgG autoantibodies. These results establish the importance of B cells and adaptive immunity in insulin resistance and suggest new diagnostic and therapeutic modalities for managing the disease.
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B2 cells accumulate in obese adipose tissue where they contribute to local and systemic insulin resistance through pathogenic IgG antibodies and activation of T cells and macrophages.
“B2 cells accumulate in the obese adipose tissue where they contribute to local and systemic IR through pathogenic IgG antibodies( 45 ) and activation of T cells and macrophages.( 46 )”
From The Emerging Role of B Cells in the Pathogenesis of NAFLD (2021) · cites this paper as [45]
B2 cells produce over a hundred different antibodies associated with insulin resistance in human adipose tissue.
“In addition to cytokines, B2 cells also produce over a hundred different antibodies that have been associated with insulin resistance in human AT (8,9).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [9]
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References 44 · Cited by 1,050
- Authors
- Winer, D. A., Winer, S., Shen, L., Wadia, P. P., Yantha, J., Paltser, G., Tsui, H., Wu, P., Davidson, M. G., Alonso, M. N., Leong, H. X., Glassford, A., Caimol, M., Kenkel, J. A., Tedder, T. F., McLaughlin, T., Miklos, D. B., Dosch, H.-M., & Engleman, E. G.
- Affiliations
- Stanford University (US)
- University Health Network (CA)
- University of Toronto (CA)
- Stanford Medicine (US)
- Duke Medical Center (US)
- Corresponding author
- Winer, Daniel A
- Engleman, Edgar G
- ORCID
- Venue
- Nature Medicine
- Published
- 2011-04-17
- Volume
- 17
- Issue
- 5
- Pages
- 610-617
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3270885
- OpenAlex
- W2146957741
- Cited by
- 1,050
- References
- 44
- Citations by year
- 2026: 35 · 2025: 58 · 2024: 63 · 2023: 49 · 2022: 77 · 2021: 81 · 2020: 69 · 2019: 71 · 2018: 63 · 2017: 91 · 2016: 62 · 2015: 76 · 2014: 70 · 2013: 106 · 2012: 55
- FWCI
- 60.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (111156)
- National Cancer Institute (CA141468, U01CA141468)
- National Institute of Allergy and Infectious Diseases (T32AI007290)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK082537, R01DK080436, DK082537)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- B cells, insulin resistance, obesity, autoantibodies, T cells, macrophages, visceral adipose tissue, diet-induced obesity, anti-CD20 monoclonal antibody, impaired glucose tolerance, adaptive immunity, chronic inflammation, B-cell depletion
- MeSH terms
- Animals, Autoantibodies, Autoantigens, B-Lymphocytes, Dietary Fats, Glucose, Humans, Immunoglobulin G, Immunoglobulin mu-Chains, Inflammation, Insulin Resistance, Lymphocyte Depletion, Lymphocyte Activation, Male, Mice, Inbred C57BL, Obesity, T-Lymphocytes, Autoimmunity, Mice, Knockout, Intra-Abdominal Fat, Mice
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