Prolonged proinflammatory cytokine production in monocytes modulated by interleukin 10 after influenza vaccination in older adults
Open accessAbstract
We evaluated in vivo innate immune responses in monocyte populations from 67 young (aged 21-30 years) and older (aged ≥65 years) adults before and after influenza vaccination. CD14(+)CD16(+) inflammatory monocytes were induced after vaccination in both young and older adults. In classical CD14(+)CD16(-) and inflammatory monocytes, production of tumor necrosis factor α and interleukin 6, as measured by intracellular staining, was strongly induced after vaccination. Cytokine production was strongly associated with influenza vaccine antibody response; the highest levels were found as late as day 28 after vaccination in young subjects and were substantially diminished in older subjects. Notably, levels of the anti-inflammatory cytokine interleukin 10 (IL-10) were markedly elevated in monocytes from older subjects before and after vaccination. In purified monocytes, we found age-associated elevation in phosphorylated signal transducer and activator of transcription-3, and decreased serine 359 phosphorylation of the negative IL-10 regulator dual-specificity phosphatase 1. These findings for the first time implicate dysregulated IL-10 production in impaired vaccine responses in older adults.
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Monocytes in older individuals produce more IL-10 after influenza vaccination, which inversely correlates with antibody titer increase.
“monocytes in older individuals produce more IL-10 after influenza vaccination, which inversely correlated with the increase in antibody titers”
From Successful and Maladaptive T Cell Aging (2017) · cites this paper as Mohanty et al., 2015
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References 38 · Cited by 67
Research works printed but not linked: 1
- Brondello JM, Pouyssegur J, McKenzie FR. Reduced MAP kinase phos- phatase-1 degradation after p42/p44MAPK-dependent phosphoryla- tion. Science 1999; 286:2514-7.
- Authors
- Mohanty, S., Joshi, S. R., Ueda, I., Wilson, J., Blevins, T. P., Siconolfi, B., Meng, H., Devine, L., Raddassi, K., Tsang, S., Belshe, R. B., Hafler, D. A., Kaech, S. M., Kleinstein, S. H., Trentalange, M., Allore, H. G., & Shaw, A. C.
- Affiliations
- Saint Louis University (US)
- Yale University (US)
- Corresponding author
- Mohanty, Subhasis
- ORCID
- Venue
- Journal of Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-11-02
- Volume
- 211
- Issue
- 7
- Pages
- 1174-1184
- ISSN
- 0022-1899 (ISSN-L)
- 1537-6613
- PMC
- PMC4366602
- OpenAlex
- W2169577121
- Cited by
- 67
- References
- 38
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 9 · 2021: 4 · 2020: 6 · 2019: 10 · 2018: 5 · 2017: 7 · 2016: 7 · 2015: 7 · 2013: 1
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Infectious Diseases (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Yale University
- National Institutes of Health (UL1TR000142)
- National Institute on Aging (K24AG042489, P30AG021342)
- National Institute of Allergy and Infectious Diseases (AI 089992, U19AI089992)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- influenza vaccination, older adults, monocytes, IL-10, inflammatory cytokines, TNF-α, interleukin-6, innate immune response, vaccine antibody response, STAT3 phosphorylation
- MeSH terms
- Adult, Age Factors, Aged, Female, Gene Expression Regulation, Humans, Immunity, Innate, Influenza, Human, Influenza Vaccines, Male, Monocytes, Phosphorylation, Tumor Necrosis Factor-alpha, Vaccination, Signal Transduction, Interleukin-6, Cytokines, Interleukin-10, Receptors, IgG, Lipopolysaccharide Receptors, STAT3 Transcription Factor, Dual Specificity Phosphatase 1, Young Adult, GPI-Linked Proteins
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