Cell signaling and the aging of B cells
Abstract
The uniqueness of each B cell lies in the structural diversity of the B-cell antigen receptor allowing the virtually limitless recognition of antigens, a necessity to protect individuals against a range of challenges. B-cell development and response to stimulation are exquisitely regulated by a group of cell surface receptors modulating various signaling cascades and their associated genetic programs. The effects of these signaling pathways in optimal antibody-mediated immunity or the aberrant promotion of immune pathologies have been intensely researched in the past in young individuals. In contrast, we are only beginning to understand the contribution of these pathways to the changes in B cells of old organisms. Thus, critical transcription factors such as E2A and STAT5 show differential expression or activity between young and old B cells. As a result, B-cell physiology appears altered, and antibody production is impaired. Here, we discuss selected phenotypic changes during B-cell aging and attempt to relate them to alterations of molecular mechanisms.
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Age-related remodeling of the B cell compartment may be the result of unbalanced fate selection in the hematopoietic progenitor cell population, autonomous changes in B cells, and external signals.
“The age-related remodeling of the B cell compartment may be the result of unbalanced fate selection in the hematopoietic progenitor cell population, autonomous changes in B cells, and external signals [138, 139].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [139]
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Immunosenescence: a key player in cancer development
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- Authors
- Labi, V., & Derudder, E.
- Affiliations
- Innsbruck Medical University (AT)
- Universität Innsbruck (AT)
- Corresponding author
- Labi, Verena
- Derudder, Emmanuel
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2020-09
- Volume
- 138
- Pages
- 110985
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W3033830318
- Cited by
- 9
- References
- 141
- Citations by year
- 2025: 2 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 2
- FWCI
- 0.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ingrid Shaker Nessmann Cancer Research Association (D-182400-020-012)
- Tyrolean Science Fund (UNI-0404/1696, UNI-0404/2310)
- Austrian Cancer Aid (KH15017)
- Austrian Science Fund (P32755)
- University Innsbruck Nachwuchsförderung (2017/BIO-5)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- B cell aging, B cell receptor signaling, signal transduction, E2A, STAT5, transcription factors, antibody production, immunosenescence, B cell development, immunopathology, aging
- MeSH terms
- Aging, B-Lymphocytes, Humans, Lymphocyte Activation, Receptors, Antigen, B-Cell, Signal Transduction
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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