Evidence map›Paper›PMID 22565047›Full record

ReviewCurrent opinion in immunology2012

Chronic inflammation and aging: DNA damage tips the balance.

Mary M Cavanagh, Cornelia M Weyand, Jörg J Goronzy

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Endothelial Dysfunction with Aging: Does Sex Matter?International journal of molecular sciences · 2024
    Article
  5. Article
  6. Review
  7. Senescent CD8Cancer science · 2023
    Article
  8. DNA polymerase κ suppresses inflammation and inflammation-induced mutagenesis and carcinogenic potential in the colon of mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
    Article
  9. Article
  10. Article
  11. Functional genomics of inflamm-aging and immunosenescence.Briefings in functional genomics · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Immunological Aspects of Skin Aging in Atopic Dermatitis.International journal of molecular sciences · 2021
    Review
  19. Human Susceptibility to Influenza Infection and Severe Disease.Cold Spring Harbor perspectives in medicine · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Mary M CavanaghDepartment of Medicine, Stanford University, Stanford, CA 94305, United States.
Cornelia M Weyand
Jörg J Goronzy
Stanford University · US

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 1998 to 2013
$20.7M
Vaccination and infection: indicators of immunological health and responsivenessU19AI090019 · NIAID · STANFORD UNIVERSITY · PI DAVIS, MARK MORRIS · 2010 to 2015
$17.3M
REGULATION OF VASCULAR FUNCTION BY THE ENDOTHELIUMR01HL039006 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 1987 to 2017
$5.5M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
OCULAR DISEASE IN GIANT CELL ARTERITISR01EY011916 · NEI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1997 to 2011
$2.9M
NEI NIH HHS R01 EY011916NEI NIH HHS R01 EY11916NHLBI NIH HHS P01 HL058000NHLBI NIH HHS R01 HL039006NHLBI NIH HHS R01 HL117913NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI44142NIAID NIH HHS U19 AI057266NIAID NIH HHS U19 AI090019NIAID NIH HHS U19 AI 57266NIAMS NIH HHS R01 AR042527NIAMS NIH HHS R01 AR42527
6 · The paper itself

Abstract

The aged immune system, typically hyporesponsive to infection and vaccination, can be hyperresponsive in the context of inflammatory pathology. Here we review current work examining the mechanisms behind the amplified inflammatory profile of aged adaptive immunity, and the reciprocal relationship between chronic inflammation and immune aging. Aged hematopoietic stem cells are driven to differentiate following accumulated DNA damage, thus depleting the stem cell pool and increasing the number of damaged effector cells in the circulation. Chronic DNA damage responses in lymphocytes as well as senescent cells of other lineages initiate the production of inflammatory mediators. In addition, aged lymphocytes become less reliant on specific antigen for stimulation and more prone to activation through innate receptors. When these lymphocytes are exposed to inflammatory signals produced by senescent tissues, the bias toward inflammation exacerbates destruction without necessarily improving immunity.

Indexed as

DNA DamageAnimalsCellular SenescenceChronic DiseaseHumansImmune SystemImmunityInflammationLymphocytes

Identifiers

PMID22565047
PMCPMC3423478
OpenAlexW1977408830

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.