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Cited by 115T-cell and B-cell ImmunologyImmune responses and vaccinationsImmune Response and Inflammation

High TNF-α levels in resting B cells negatively correlate with their response

Open access
Frasca, Daniela, Diaz, Alain, Romero, Maria, Landin, Ana Marie, Blomberg, Bonnie B.·2014·Experimental Gerontology
DOI 10.1016/j.exger.2014.01.004PMC PMC3989457
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Abstract

Aging significantly decreases the influenza vaccine-specific response as we and others have previously shown. Based on our previous data in aged mice, we hypothesize that the inflammatory status of the individual and of B cells themselves would impact B cell function. We here show that the ability to generate a vaccine-specific antibody response is negatively correlated with levels of serum TNF-α. Moreover, human unstimulated B cells from elderly make higher levels of TNF-α than those from young individuals, and these positively correlate with serum TNF-α levels. These all negatively correlate with B cell function, measured by activation-induced cytidine deaminase, the enzyme of class switch recombination and somatic hypermutation. Only memory B cells (either IgM or switched), but not naïve B cells, make appreciable levels of TNF-α and more in elderly as compared to young individuals. Finally, an anti-TNF-α antibody can increase the response in cultured B cells from the elderly, suggesting that TNF-α secreted by memory B cells affects IgM memory B cells and naïve B cells in an autocrine and/or paracrine manner. Our results show an additional mechanism for reduced B cell function in the elderly and propose B cell-derived TNF-α as another predictive biomarker of in vivo and in vitro B cell responses.

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Crossref · 10.1016/j.exger.2014.01.004

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  • Inflammaging drives TNF-α expression in B cells from elderly individuals, and these levels are positively correlated with serum TNF-α and negatively correlated with the response of the same B cells after in vitro stimulation, measured by AID.

    “Inflammaging not only induces higher expression of inflammatory miRs, but has also been shown to drive TNF-α expression in B cells from elderly individuals, and these levels are positively correlated with serum TNF-α and negatively correlated with the response of the same B cells after in vitro stimulation, which is measured by AID [121].”

    From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [121]

  • Age-related intrinsic B-cell defects responsible for sub-optimal antibody responses in elderly to infections and vaccines have been identified.

    “Age-related intrinsic B-cell defects, responsible for sub-optimal antibody responses in elderly individuals to infections and vaccines have been identified [95, 121–123]”

    From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [121]

  • These intrinsic B-cell defects include decreases in expression and function of the transcription factor E47.

    “and include decreases in expression and function of the key transcription factor E47 (see below), along with a reduction in activation-induced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation.”

    From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [121]

  • These intrinsic B-cell defects include a reduction in activation-induced cytidine deaminase (AID).

    “and include decreases in expression and function of the key transcription factor E47 (see below), along with a reduction in activation-induced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation.”

    From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [121]

  • The receptor antagonist IL-1ra is increased after sleep deprivation in humans and animals.

    “The receptor antagonist IL-1ra, which is a natural inhibitor of IL-1 signaling, was increased after sleep deprivation in humans and animals (200, 245).”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [200]

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Authors
Frasca, D., Diaz, A., Romero, M., Landin, A. M., & Blomberg, B. B.
Affiliations
University of Miami (US)
Corresponding author
Frasca, Daniela
ORCID
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2014-06
Volume
54
Pages
116-122
ISSN
0531-5565 (ISSN-L)
DOI
10.1016/j.exger.2014.01.004
PMC
PMC3989457
OpenAlex
W1975653620
Cited by
115
References
57
Citations by year
2026: 9 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 13 · 2021: 20 · 2020: 14 · 2019: 9 · 2018: 4 · 2017: 8 · 2016: 10 · 2015: 6 · 2014: 3
FWCI
4.11
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
NIH (AG-32576, 5R21AI096446-02, 1R21AG042826-01)
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 › Immune Response and Inflammation
Keywords
TNF-α, B cells, aging, influenza vaccine response, memory B cells, naive B cells, activation-induced cytidine deaminase, class switch recombination, somatic hypermutation, anti-TNF-alpha antibody, autocrine and paracrine signaling, B cell function
MeSH terms
Adult, Aged, B-Lymphocytes, Cells, Cultured, Female, Humans, Immunologic Memory, Influenza Vaccines, Lipopolysaccharides, Male, Middle Aged, RNA, Messenger, Tumor Necrosis Factor-alpha, Young Adult

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