ArticleFrontiers in immunology2017
Old Mice Accumulate Activated Effector CD4 T Cells Refractory to Regulatory T Cell-Induced Immunosuppression.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response.Frontiers in aging · 2026Review
- Article
- Extracellular Delivery of Functional Mitochondria Rescues the Dysfunction of CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Acute inflammation alters lung lymphocytes and potentiates innate-like behavior in young mouse lung CD8 T cells, resembling lung CD8 T cells from old mice.Journal of leukocyte biology · 2023Article
- N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer's disease mouse model.Nature communications · 2023Article
- Immune phenotype of the CD4GeroScience · 2022Article
- T cell cholesterol efflux suppresses apoptosis and senescence and increases atherosclerosis in middle aged mice.Nature communications · 2022Article
- Inflammation, Immune Senescence, and Dysregulated Immune Regulation in the Elderly.Frontiers in aging · 2022Review
- Effects of zinc status on age-related T cell dysfunction and chronic inflammation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021Article
- The Role of Dectin-1 Signaling in Altering Tumor Immune Microenvironment in the Context of Aging.Frontiers in oncology · 2021Article
- Rapamycin Eyedrops Increased CD4International journal of molecular sciences · 2020Article
- Loss of BIM in T cells results in BCL-2 family BH3-member compensation but incomplete cell death sensitivity normalization.Apoptosis : an international journal on programmed cell death · 2020Article
- Syngeneic red blood cell-induced extracellular vesicles suppress delayed-type hypersensitivity to self-antigens in mice.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Article
- Aging promotes reorganization of the CD4 T cell landscape toward extreme regulatory and effector phenotypes.Science advances · 2019Article
- CD4 T Cells Induce A Subset of MHCII-Expressing Microglia that Attenuates Alzheimer Pathology.iScience · 2019Article
- Age-related Autoimmune Changes in Lacrimal Glands.Immune network · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic low-grade inflammation and reduced lymphocyte potency are implicated in the pathogenesis of major illnesses associated with aging. Whether this immune phenotype results from a loss of cell-mediated regulation or intrinsic dysregulated function of effector T cells (Teffs) requires further research. Here, we report that, as compared with young C57BL6 mice, old mice show an increased frequency of CD4+CD62L- Teffs with a dysregulated activated phenotype and markedly increased effector functions. Analysis of the frequency and suppressive function of CD4+FoxP3+ regulatory T cells (Tregs) indicates an increase in the frequency of FoxP3+ T cells with aging which, however, occurs within the CD4+CD25- T cells. Furthermore, whereas Tregs from young and old mice similarly suppress Teffs from young mice, both have a compromised suppressive capacity of Teffs from old mice, a phenomenon which is partially recovered in the presence of IL-2-producing CD4+CD62L+ non-Teffs. Finally, we observed that Teff subsets from old mice are enriched with IL-17A-producing T cells and exhibit intrinsically dysregulated expression of genes encoding cell-surface molecules and transcription factors, which play a key role in T-cell activation and regulation. We, thus, demonstrate an age-related impairment in the regulation of effector CD4 T cells, which may underlie the higher risk for destructive inflammation associated with aging.
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