Age-Associated B Cells: A T-bet–Dependent Effector with Roles in Protective and Pathogenic Immunity
Open accessAbstract
A newly discovered B cell subset, age-associated B cells, expresses the transcription factor T-bet, has a unique surface phenotype, and accumulates progressively with age. Moreover, B cells with these general features are associated with viral infections and autoimmunity in both mice and humans. In this article, we review current understanding of the characteristics, origins, and functions of these cells. We also suggest that the protective versus pathogenic actions of these cells reflect appropriate versus aberrant engagement of regulatory mechanisms that control the Ab responses to nucleic acid–containing Ags.
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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 [25]
The sections on ABC characteristics and accumulation with age (page not provided) identify CD11c-positive, T-bet-dependent ABCs and link their accumulation to aging and autoimmunity. The paper does not establish that ABCs are key regulators of immune tolerance, and the passages found do not address Tregs or the effects of Treg loss. It suggests that elevated inflammatory cytokines may promote ABC expansion, rather than establishing that ABC expansion causes chronic inflammation. (LLM, conf=0.88)
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- Authors
- Rubtsova, K., Rubtsov, A. V., Cancro, M. P., & Marrack, P.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of Pennsylvania (US)
- Corresponding author
- Rubtsova, Kira
- Marrack, Philippa
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-09-01
- Volume
- 195
- Issue
- 5
- Pages
- 1933-1937
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC4548292
- OpenAlex
- W2120679720
- Cited by
- 246
- References
- 57
- Citations by year
- 2026: 21 · 2025: 27 · 2024: 11 · 2023: 22 · 2022: 28 · 2021: 32 · 2020: 25 · 2019: 33 · 2018: 17 · 2017: 19 · 2016: 10 · 2015: 1
- FWCI
- 1.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute on Aging (R01AG-16841, R01AG016841)
- National Institute of Allergy and Infectious Diseases (AI-18785, T32AI074491, R37AI018785, R56AI018785, R01AI118691, R01AI018785)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- age-associated B cells, T-bet, B cell differentiation, aging, autoimmunity, viral infection, antibody response, B-cell origin, protective immunity
- MeSH terms
- T-bet Transcription Factor, Aging, Animals, Humans, Inflammation, Signal Transduction, Autoimmunity, B-Lymphocyte Subsets, Models, Immunological, T-Box Domain Proteins, Mice
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