ArticleAging cell2022
B cell-intrinsic changes with age do not impact antibody-secreting cell formation but delay B cell participation in the germinal centre reaction.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- The ageing immune system as a driver of systemic ageing.Nature reviews. Immunology · 2026Review
- IL-2 silencing enables Tfh cell expansion during vaccination but is redundant for antibody production.Immunology and cell biology · 2026Article
- Extrafollicular and other non-germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Mesenchymal stromal cells counteract with age-related immune decline and enhance vaccine efficacy by modulating endogenous splenic marginal reticular cells in elderly models.Cellular & molecular immunology · 2026Article
- CD21Frontiers in aging · 2026Article
- Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response.Frontiers in aging · 2026Review
- Aging and immunity: the age-old tango.Genes & development · 2025Review
- Germinal center immune dynamics: challenges for effective vaccination in the elderly.Immunotherapy · 2025Review
- Enhancing thymic function improves T-cell reconstitution and immune responses in aged mice.PLoS biology · 2025Article
- Sustained mTORC1 activation in activated T cells impairs vaccine responses in older individuals.Science advances · 2025Article
- Old hematopoietic stem cells retain competence to reconstitute a youthful B cell system that is highly responsive to protein-based vaccination.Immunity & ageing : I & A · 2025Article
- Exponential decline, ceiling effect, downregulation, and T-cell response in immunoglobulin G antibody levels after messenger RNA vaccine boosters: a case report.Journal of medical case reports · 2024Article
- The role of autoantibodies in bridging obesity, aging, and immunosenescence.Immunity & ageing : I & A · 2024Review
- Immunosenescence: Aging and Immune System Decline.Vaccines · 2024Review
- SARS-CoV-2 and innate immunity: the good, the bad, and the "goldilocks".Cellular & molecular immunology · 2024Review
- Systemic immunometabolism and responses to vaccines: insights from T and B cell perspectives.International immunology · 2023Review
- Depletion of preexisting B-cell lymphoma 2-expressing senescent cells before vaccination impacts antigen-specific antitumor immune responses in old mice.Aging cell · 2023Article
- B Cells from Aged Mice Do Not Have Intrinsic Defects in Affinity Maturation in Response to Immunization.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- TNF is a critical cytokine in age-related dry eye disease.The ocular surface · 2023Article
- Severe respiratory viral infections: T-cell functions diverging from immunity to inflammation.Trends in microbiology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Vaccines typically protect against (re)infections by generating pathogen-neutralising antibodies. However, as we age, antibody-secreting cell formation and vaccine-induced antibody titres are reduced. Antibody-secreting plasma cells differentiate from B cells either early post-vaccination through the extrafollicular response or from the germinal centre (GC) reaction, which generates long-lived antibody-secreting cells. As the formation of both the extrafollicular antibody response and the GC requires the interaction of multiple cell types, the impaired antibody response in ageing could be caused by B cell intrinsic or extrinsic factors, or a combination of the two. Here, we show that B cells from older people do not have intrinsic defects in their proliferation and differentiation into antibody-secreting cells in vitro compared to those from the younger donors. However, adoptive transfer of B cells from aged mice to young recipient mice showed that differentiation into extrafollicular plasma cells was favoured at the expense of B cells entering the GC during the early stages of GC formation. In contrast, by the peak of the GC response, GC B cells derived from the donor cells of aged mice had expanded to the same extent as those from the younger donors. This indicates that age-related intrinsic B cell changes delay the GC response but are not responsible for the impaired antibody-secreting response or smaller peak GC response in ageing. Collectively, this study shows that B cells from aged individuals are not intrinsically defective in responding to stimulation and becoming antibody-secreting cells, implicating B cell-extrinsic factors as the primary cause of age-associated impairment in the humoral immunity.
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Registered trials
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