Aging is associated with a numerical and functional decline in plasmacytoid dendritic cells, whereas myeloid dendritic cells are relatively unaltered in human peripheral blood
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Dendritic cells (DC) are potent antigen-presenting cells that initiate and regulate T-cell responses. In this study, the numbers and functional cytokine secretions of plasmacytoid and myeloid DC (pDC and mDC, respectively) in peripheral blood from young and elderly subjects were compared. Overall, pDC numbers in peripheral blood were lower in healthy elderly compared with healthy young subjects (p = 0.016). In response to influenza virus stimulation, isolated pDC from healthy elderly subjects secreted less interferon (IFN)-alpha compared with those from healthy young subjects. The decline in IFN-alpha secretion was associated with a reduced proportion of pDC that expressed Toll-like receptor-7 or Toll-like receptor-9. In contrast, there was little difference in the numbers and cytokine secretion function between healthy young and healthy elderly subjects (p = 0.82). However, in peripheral blood from frail elderly subjects, the numbers of mDC were severely depleted as compared with either healthy young or elderly subjects (p = 0.014 and 0.007, respectively). Thus, aging was associated with the numerical and functional decline in pDC, but not mDC, in healthy young versus elderly subject group comparisons, while declining health in the elderly can profoundly impact mDC negatively. Because of the importance of pDC for antiviral responses, the age-related changes in pDC likely contribute to the impaired immune response to viral infections in elderly persons, especially when combined with the mDC dysfunction occurring in those with compromised health.
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Elderly people have a diminished capacity to produce type I interferons.
“have diminished capacity to produce type I IFNs119-121.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [121]
pDCs from elderly subjects show marked impairment of pro-inflammatory cytokine release upon viral or TLR stimulation, with reduced intracellular TNF-α, IL-6, IL-12, IFN-α, IFN-β and IFN-γ, but phagocytosis appears well preserved.
“pDCs are characterized by a marked impairment of pro-inflammatory cytokine release with aging: pDCs display a reduction in intracellular levels of TNF-α, IL-6 and IL-12, as well as IFN-α, IFN-β and IFN-γ upon viral or TLR stimulation [52, 53]; however, phagocytosis appears well preserved [41].”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [53]
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- Authors
- Jing, Y., Shaheen, E., Drake, R. R., Chen, N., Gravenstein, S., & Deng, Y.
- Affiliations
- Eastern Virginia Medical School (US)
- Corresponding author
- Deng, Yuping
- Venue
- Human Immunology
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 70
- Issue
- 10
- Pages
- 777-784
- ISSN
- 0198-8859 (ISSN-L)
- PMC
- PMC5718338
- OpenAlex
- W2091790511
- Cited by
- 284
- References
- 53
- Citations by year
- 2026: 11 · 2025: 22 · 2024: 21 · 2023: 11 · 2022: 20 · 2021: 32 · 2020: 18 · 2019: 17 · 2018: 14 · 2017: 21 · 2016: 15 · 2015: 13 · 2014: 14 · 2013: 24 · 2012: 14
- FWCI
- 4.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Human Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Commonwealth Health Research Board
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- dendritic cells, plasmacytoid dendritic cells, myeloid dendritic cells, aging, frailty, interferon-alpha, TLR7, TLR9, influenza virus, antiviral immunity, peripheral blood, older adults
- MeSH terms
- Adult, Aged, Aged, 80 and over, Aging, Cell Count, Dendritic Cells, Humans, Middle Aged, Cytokines, Interferon-alpha, Myeloid Cells, Toll-Like Receptor 7, Toll-Like Receptor 9
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