Age-associated B cells in autoimmune diseases
Open accessAbstract
Age-associated B cells (ABCs) are a transcriptionally and functionally unique B cell population. In addition to arising with age and following infection, ABCs are expanded during autoimmune disease, including those with systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. The exact nature of how ABCs impact disease remains unclear. Here, we review what is known regarding ABC development and distribution during diseases including systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. We discuss possible mechanisms by which ABCs could contribute to disease, including the production of cytokines and autoantibodies or stimulation of T cells. Finally, we speculate on how ABCs might act as mediators between sex, infection, and autoimmune disease, and discuss avenues for further research.
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Age-associated B cells (ABCs; CD11c+T-bet+) and regulatory T cells (Tregs) are key regulators of immune tolerance in aging, and their expansion or loss, respectively, has been implicated in age-related autoimmunity and chronic inflammation.
“Age-associated B cells (ABCs; CD11c+T-bet+) and regulatory T cells (Tregs) are key regulators of immune tolerance in aging, and their expansion or loss, respectively, has been implicated in age-related autoimmunity and chronic inflammation [25–29].”
From PLCγ2 deficiency compromises systemic immune tolerance and erodes myelin homeostasis while enhancing oxidative metabolism in the mouse brain (2026) · cites this paper as [26]
The Introduction and “Frequency of ABCs is increased during autoimmunity” sections identify ABCs using T-bet and CD11c and report their expansion with aging and in autoimmune disease. The “ABCs and tolerance” section discusses possible protective as well as pathogenic roles, but does not establish ABCs as key regulators of tolerance in aging. The copy does not support the claim about age-related Treg loss or its link to chronic inflammation; a reference title mentions regulatory T cells in patients with common variable immunodeficiency, not aging. (LLM, conf=0.88)
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Non-apoptotic FAS signaling controls mTOR activation and extrafollicular maturation in human B cells
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Autoantibodies to Interferons in Infectious Diseases
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- Authors
- Mouat, I. C., Goldberg, E., & Horwitz, M. S.
- Affiliations
- University of British Columbia (CA)
- Corresponding author
- Horwitz, Marc S.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2022-07-07
- Volume
- 79
- Issue
- 8
- Pages
- 402-402
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC9263041
- OpenAlex
- W4284886126
- Cited by
- 170
- References
- 95
- Citations by year
- 2026: 29 · 2025: 50 · 2024: 57 · 2023: 28 · 2022: 6
- FWCI
- 3.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Multiple Sclerosis Scientific Research Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- age-associated B cells, autoimmune disease, systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis, autoantibodies, cytokine production, T cell stimulation, B cell development, sex differences, infection, aging
- MeSH terms
- Arthritis, Rheumatoid, Autoantibodies, Autoimmune Diseases, Humans, Lupus Erythematosus, Systemic, Multiple Sclerosis
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