B cells and aging: Balancing the homeostatic equation
Open accessAbstract
The interplay of selective and homeostatic processes dominates the behavior of B lineage subsets following B cell antigen receptor (BCR) expression, and extends to determinants of immune response quality and the persistence of immunologic memory. A key concept emerging from these considerations is that primary events acting upstream of mature B lymphocyte pools can profoundly impact downstream populations as the system attempts homeostatic adjustments. Since, advancing age is accompanied by profound changes in B cell generation and homeostasis, establishing the relative contributions of primary lesions versus compensatory homeostatic processes is critical to understanding these perturbations. Exploration of this problem requires an understanding of: (1) the identity, dynamics, and progenitor/successor relationships of marrow and peripheral B cell subsets; (2) the nature and interactions of selective and homeostatic processes acting in these subsets; (3) how these change with age. Our data show that BLyS and its receptors mediate peripheral B cell homeostasis, and that the size, dynamics and behavior of all B cell subsets influenced by B Lymphocyte Stimulator change with age. These findings suggest that homeostatic processes mediated through B Lymphocyte Stimulator are altered with age, and that these perturbations may primarily reflect compensatory homeostatic adjustments to upstream reductions in B cell generation.
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Some age-related B cell deficiencies may occur secondary to T cell deficiencies.
“In view of the critical role played by CD4 + T cells in orchestrating the immune response, some of the age-related deficiencies observed in B cells (51,53,54), which include a reduction in the number of plasmablasts that develop in response to influenza vaccination (55) and the production of poor-quality antibodies to carbohydrate antigens (56)(57)(58), may occur secondary to T cell deficiencies.”
From Causes, consequences, and reversal of immune system aging (2013) · cites this paper as [54]
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- Authors
- MILLER, J., & CANCRO, M.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- CANCRO, M
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 42
- Issue
- 5
- Pages
- 396-399
- ISSN
- 0531-5565 (ISSN-L)
- PMC
- PMC1952233
- OpenAlex
- W2014770456
- Cited by
- 67
- References
- 24
- Citations by year
- 2025: 5 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 7 · 2020: 5 · 2019: 6 · 2018: 2 · 2017: 6 · 2014: 5 · 2013: 5 · 2012: 5
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Public Health Service
- National Institute on Aging (R01AG030227, AG-R01-16841, R01AG016841)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- B cell homeostasis, aging, B lymphocyte stimulator, B cell subsets, B cell receptor, immunological memory, B cell progenitors, peripheral blood B cells
- MeSH terms
- Aging, B-Lymphocytes, Homeostasis, Humans, B-Lymphocyte Subsets, Precursor Cells, B-Lymphoid
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