ArticleAging cell2017
Aging-associated dysregulation of homeostatic immune response termination (and not initiation).
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Integrated Bioinformatic Identification and Experimental Validation Reveal That Aging Exacerbates ARDS Through MAPK14/ADM/MAPK8 Axis.Journal of inflammation research · 2026Article
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.Cancer biology & medicine · 2025Review
- Effects of Silibinin on Delaying Aging inAntioxidants (Basel, Switzerland) · 2025Article
- Extracellular Delivery of Functional Mitochondria Rescues the Dysfunction of CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Macrophages in Lung Repair and Fibrosis.Results and problems in cell differentiation · 2024Review
- Anti-Inflammatory Klotho Protein Serum Concentration Correlates with Interferon Gamma Expression Related to the Cellular Activity of Both NKT-like and T Cells in the Process of Human Aging.International journal of molecular sciences · 2023Article
- IL-34 Downregulation‒Associated M1/M2 Macrophage Imbalance Is Related to Inflammaging in Sun-Exposed Human Skin.JID innovations : skin science from molecules to population health · 2022Article
- Solving neurodegeneration: common mechanisms and strategies for new treatments.Molecular neurodegeneration · 2022Review
- A potential association between immunosenescence and high COVID-19 related mortality among elderly patients with cardiovascular diseases.Immunity & ageing : I & A · 2021Review
- Neuroinflammation in Alzheimer's Disease.Biomedicines · 2021Review
- Dysregulation of Systemic Immunity in Aging and Dementia.Frontiers in cellular neuroscience · 2021Review
- Dysfunction of B Cell Leading to Failure of Immunoglobulin Response Is Ameliorated by Dietary Silk Peptide in 14-Month-Old C57BL/6 Mice.Frontiers in nutrition · 2020Article
- Nontuberculous mycobacterium M. avium infection predisposes aged mice to cardiac abnormalities and inflammation.Aging cell · 2019Article
- Effect of Systemic Inflammation on Rat Attentional Function and Neuroinflammation: Possible Protective Role for Food Restriction.Frontiers in aging neuroscience · 2019Article
- Apoptotic cells enhance pathogenesis of Listeria monocytogenes.Microbial pathogenesis · 2017Article
- Association between temporal trajectories of inflammatory markers and prognosis in ischemic stroke.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Immunosenescence is a state of unbalanced immune responsiveness, characterized by a diverse repertoire of seemingly discreet and paradoxical alterations in all aspects of immunity arising in an aging-associated manner. We asked whether aging-associated alterations in the ability of apoptotic cells to elicit immunomodulatory responses (innate apoptotic immunity; IAI) or in IAI responses themselves might underlie the confounding aging-associated anomalies of immunosenescence. We explored this question by examining, as a function of animal age, responsiveness of murine macrophages on the single cell level. We monitored the expression of pro- and anti-inflammatory cytokines cytofluorimetrically in response to pro-inflammatory Toll-like receptor (TLR) stimulation and anti-inflammatory treatment with apoptotic cells. While we found no alterations with age in the potency of apoptotic cells or in the initiation and magnitude of IAI responses, we did identify a cell-intrinsic deficiency in anti-inflammatory IAI response termination linked with age and preceding manifestations of immunosenescence. Further, we found that an aging-associated deficiency in response termination also is evident following TLR stimulation. These surprising observations reveal that a loss of homeostatic immune control with animal age results from the dysregulation of response termination (as distinct from response initiation) and is exerted on the level of transcription. We suggest that, with advancing age, cells become locked into relatively longer-lived response states. Aging-associated immune dysfunctions may reflect a diminution in the cellular nimbleness of immune responsiveness.
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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.