ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Aging mice exhibit a functional defect in mucosal dendritic cell response against an intracellular pathogen.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed.
- Respiratory virus immune response in the aged host.Immunity & ageing : I & A · 2026Review
- Unwanted disorders and xenogeneic graft-versus-host disease in experimental immunodeficient mice: How to evaluate and how to report.Animal models and experimental medicine · 2025Review
- Immune Response to Chikungunya Virus: Sex as a Biological Variable and Implications for Natural Delivery via the Mosquito.Viruses · 2023Review
- Immunosenescence and multiple sclerosis: inflammaging for prognosis and therapeutic consideration.Frontiers in aging · 2023Review
- Chronically hypertensive transgenic mice expressing human AT1R haplotype-I exhibit increased susceptibility toFrontiers in microbiology · 2023Article
- Review
- A gut-centric view of aging: Do intestinal epithelial cells contribute to age-associated microbiota changes, inflammaging, and immunosenescence?Aging cell · 2022Review
- The accumulation of Vγ4 T cells with aging is associated with an increased adaptive Vγ4 T cell response after foodborne Listeria monocytogenes infection of mice.Immunity & ageing : I & A · 2022Article
- Immune checkpoint expression and relationships to anti-PD-L1 immune checkpoint blockade cancer immunotherapy efficacy in aged versus young mice.Aging and cancer · 2022Article
- Immune Response to Microsporidia.Experientia supplementum (2012) · 2022Article
- The impact of aging on intestinal mucosal immune function and clinical applications.Frontiers in immunology · 2022Review
- Gut microbiota alterations and health status in aging adults: From correlation to causation.Aging medicine (Milton (N.S.W)) · 2021Review
- Review
- Review
- Article
- Rejuvenating conventional dendritic cells and T follicular helper cell formation after vaccination.eLife · 2020Article
- Innate and Adaptive Immune Responses Against Microsporidia Infection in Mammals.Frontiers in microbiology · 2020Review
- Diminished immune responses with aging predispose older adults to common and uncommon influenza complications.Cellular immunology · 2019Review
- The Lung Mucosa Environment in the Elderly Increases Host Susceptibility to Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2019Article
- Influenza Pathogenesis: The Effect of Host Factors on Severity of Disease.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Down-regulation of the immune response in aging individuals puts this population at a potential risk against infectious agents. In-depth studies conducted in humans and mouse models have demonstrated that with increasing age, the T cell immune response against pathogens is compromised and response to vaccinations is subdued. In the present study, using a mouse model, we demonstrate that older animals exhibit greater susceptibility to Encephalitozoon cuniculi infection, and their ability to evoke an Ag-specific T cell response at the gut mucosal site is reduced. The dampening of T cell immunity was due to the defective priming by the dendritic cells (DC) isolated from the mucosal tissues of aging animals. When primed with DC from younger mice, T cells from older animals were able to exhibit an optimal Ag-specific response. The functional defect in DC from older mice can be attributed to a large extent to reduced IL-15 message in these cells, which can be reversed by addition of exogenous IL-15 to the cultures. IL-15 treatment led to optimal expression of costimulatory molecules (CD80 and CD86) on the surface of older DC and restored their ability to prime a T cell response against the pathogen. To our knowledge, this is the first report which demonstrates the inability of the DC population from aging animals to prime a robust T cell response against an infectious agent. Moreover, the observation that IL-15 treatment can reverse this defect has far-reaching implications in developing strategies to increase vaccination protocols for aging populations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.