CoChat
Sign Up
Cited by 339Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceT-cell and B-cell Immunology

The DOI matches its Crossref record; 419 of the 419 references it cites were found in a registry or an index.

Aging and Immune Function: Molecular Mechanisms to Interventions

Open access
Ponnappan, Subramaniam, Ponnappan, Usha·2011·Antioxidants & Redox Signaling
DOI 10.1089/ars.2010.3228PMC PMC3061194
Open this paper in CoChat — free account

Abstract

Abstract The immune system of an organism is an essential component of the defense mechanism aimed at combating pathogenic stress. Age-associated immune dysfunction, also dubbed "immune senescence," manifests as increased susceptibility to infections, increased onset and progression of autoimmune diseases, and onset of neoplasia. Over the years, extensive research has generated consensus in terms of the phenotypic and functional defects within the immune system in various organisms, including humans. Indeed, age-associated alterations such as thymic involution, T cell repertoire skewing, decreased ability to activate naïve T cells and to generate robust memory responses, have been shown to have a causative role in immune decline. Further, understanding the molecular mechanisms underlying the generation of proteotoxic stress, DNA damage response, modulation of ubiquitin proteasome pathway, and regulation of transcription factor NFκB activation, in immune decline, have paved the way to delineating signaling pathways that cross-talk and impact immune senescence. Given the role of the immune system in combating infections, its effectiveness with age may well be a marker of health and a predictor of longevity. It is therefore believed that a better understanding of the mechanisms underlying immune senescence will lead to an effective interventional strategy aimed at improving the health span of individuals. Antioxid. Redox Signal. 14, 1551-1585.

Overview

Integrity signals

Registry

Crossref · 10.1089/ars.2010.3228

Cites

419 of 419 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 419 references

Research works printed but not linked: 2

  1. 10.1016/j.stem.2007.02.001 · DOI · Paper page
  2. Ponnappan S, , Ponnappan U. Ubiquitin-proteasome pathway in immune-senescence. Recent Research Developments in Biochemistry Vol. 4 Part II. Pandalai S. Trivandrum, India: Research Signpost, 2003; 779–785.

Cited by

Sorted by citations

Items 201–300 of 339

Related

See all

Metadata

Authors
Ponnappan, S., & Ponnappan, U.
Affiliations
University of Arkansas for Medical Sciences (US)
Corresponding author
Ponnappan, Usha
Venue
Antioxidants & Redox Signaling
Publisher
SAGE Publications
Published
2011-04
Volume
14
Issue
8
Pages
1551-1585
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
DOI
10.1089/ars.2010.3228
PMC
PMC3061194
OpenAlex
W2016256318
Cited by
339
References
419
Citations by year
2026: 8 · 2025: 32 · 2024: 40 · 2023: 28 · 2022: 27 · 2021: 49 · 2020: 25 · 2019: 22 · 2018: 26 · 2017: 26 · 2016: 16 · 2015: 10 · 2014: 7 · 2013: 13 · 2012: 6
FWCI
0.62
Type
journal article
Language
en
Open access
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG-13081, AG030599, R01AG013081, AG025220, R01AG030599, R01AG025220)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
immunosenescence, aging, thymic involution, naive T cell activation, memory T cells, proteotoxic stress, DNA damage response, ubiquitin-proteasome system, NF-κB activation, autoimmune disease, cancer susceptibility, healthspan, longevity
MeSH terms
Aging, Animals, DNA, Humans, Immune System, T-Lymphocytes, NF-kappa B, Telomere, Reactive Oxygen Species, MicroRNAs

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review