MicroRNAs miR-155 and miR-16 decrease AID and E47 in B cells from elderly individuals
Open accessAbstract
Our research in the past few years has identified B cell-specific biomarkers able to predict optimal Ab responses in both young and elderly individuals. These biomarkers are activation-induced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation; the transcription factor E47, crucial for AID expression; and the ability to generate optimal memory B cells. Moreover, we have found that the increased proinflammatory status of the elderly, both in sera and intrinsic to B cells, negatively impacts B cell function. We have now investigated whether particular inflammatory microRNAs (miRs) contribute to decreased E47 and AID in aged B cells. Our data indicate that E47 and AID mRNA stability is lower in stimulated B cells from elderly individuals. We measured the expression of two miRs crucial for class switch recombination, miR-155 and miR-16, in human unstimulated B cells from young and elderly individuals with the rationale that increases in these before stimulation would decrease E47/AID upon cell activation. We found these miRs and B cell-intrinsic inflammation upregulated in aged unstimulated B cells and negatively associated with AID in the same B cells after stimulation with CpG. We propose that the downregulation of AID in aged human B cells may occur through binding of miR-155 to the 3'-untranslated regions of AID mRNA and/or binding of miR-16 to the 3'-untranslated regions of E47 mRNA, as well as at the transcriptional level of less E47 for AID. Our results indicate novel molecular pathways leading to reduced B cell function with aging.
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The reduced levels of E47 and AID mRNA in B cells from older individuals are also due to the reduced mRNA stability.
“The reduced levels of E47 and AID mRNA in B cells from older individuals are also due to the reduced mRNA stability.”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [69]
It is due to the higher expression of the inflammatory mi-RNAs 16 and 155, which bind to the 3'-untranslated region of E47 and AID mRNA, respectively, inducing mRNA degradation.
“It is due to the higher expression of the inflammatory mi-RNAs 16 and 155, which bind to the 3'-untranslated region of E47 and AID mRNA, respectively, inducing mRNA degradation (69).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [69]
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- Authors
- Frasca, D., Diaz, A., Romero, M., Ferracci, F., & Blomberg, B. B.
- Affiliations
- University of Miami (US)
- Corresponding author
- Frasca, Daniela
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-09-01
- Volume
- 195
- Issue
- 5
- Pages
- 2134-2140
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC4546853
- OpenAlex
- W2158271393
- Cited by
- 69
- References
- 65
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 3 · 2022: 10 · 2021: 12 · 2020: 3 · 2019: 11 · 2018: 4 · 2017: 11 · 2016: 8 · 2015: 1
- FWCI
- 3.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Miami
- Sylvester Comprehensive Cancer Center, University of Miami Health Systems
- National Institutes of Health (AG-32576, AG042826)
- Leonard M. Miller School of Medicine
- National Institute on Aging (R01AG032576, R37AG023717, AG32576, AG042826, R56AG032576, R21AG042826)
- National Institute of Allergy and Infectious Diseases (R21AI096446, AI096446)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- miR-155, miR-16, microRNA, activation-induced cytidine deaminase, B cell aging, class switch recombination, somatic hypermutation, memory B cells, CpG stimulation, mRNA stability, 3' untranslated region, immunosenescence
- MeSH terms
- AICDA (Activation-Induced Cytidine Deaminase), Adult, Age Factors, Aged, B-Lymphocytes, Cells, Cultured, Cytidine Deaminase, Female, Flow Cytometry, Humans, Male, Middle Aged, RNA, Messenger, Tumor Necrosis Factor-alpha, Down-Regulation, Reverse Transcriptase Polymerase Chain Reaction, 3' Untranslated Regions, MicroRNAs, Transcription Factor 3
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