Effects of aging on B cell function
Open accessAbstract
Ability to make an optimal immune response to vaccines and infectious agents declines with age in humans and animal models. Recent advances have shown intrinsic B cell defects in aged mice and humans, including decreases in Ig class switch recombination (CSR), activation-induced cytidine deaminase (AID), and E47 transcription factor. Effects on somatic hypermutation (SHM) have been varied depending on the system studied. Increase of AID in mice has shown improved CSR but not SHM. The reported microarray analysis of human B cell subsets may now be used to delineate B cell defects with aging and all the advances presented should lead to selecting agents for improved immune response in the elderly.
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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 [51]
B cell number in mice is unchanged by aging, but in human peripheral blood the absolute number is reduced.
“B cell number in mice is unchanged by aging, but in human peripheral blood their absolute number is reduced (51).”
From Causes, consequences, and reversal of immune system aging (2013) · cites this paper as [51]
The decline in human B cell number is likely due to fewer IgM+ memory and switched memory B cells, because total naive B cells remain unchanged by aging.
“This decline is likely due to decreased numbers of IgM + memory and switched memory B cells, because the total number of naive B cells remains unchanged by aging (51,52).”
From Causes, consequences, and reversal of immune system aging (2013) · cites this paper as [51]
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- Authors
- Frasca, D., & Blomberg, B. B.
- Affiliations
- University of Miami (US)
- Corresponding author
- Blomberg, Bonnie B
- Venue
- Current Opinion in Immunology
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 21
- Issue
- 4
- Pages
- 425-430
- ISSN
- 0952-7915 (ISSN-L)
- PMC
- PMC2853364
- OpenAlex
- W1989321304
- Cited by
- 161
- References
- 59
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 2 · 2023: 8 · 2022: 17 · 2021: 9 · 2020: 21 · 2019: 7 · 2018: 7 · 2017: 5 · 2016: 8 · 2015: 7 · 2014: 8 · 2013: 14 · 2012: 13
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG-23717, AG28586)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- B cell aging, immunosenescence, activation-induced cytidine deaminase, somatic hypermutation, B cell defect, vaccine response in the elderly, aged mice
- MeSH terms
- AICDA (Activation-Induced Cytidine Deaminase), Aging, Animals, B-Lymphocytes, Cytidine Deaminase, Gene Expression Regulation, Humans, Immune Tolerance, Immunoglobulin Class Switching, Somatic Hypermutation, Immunoglobulin, Mice, TCF Transcription Factors, Transcription Factor 7-Like 1 Protein
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