Evidence map›Paper›PMID 28005419›Full record

ReviewAnnals of the American Thoracic Society2016

Aging of the Immune System. Mechanisms and Therapeutic Targets.

Cornelia M Weyand, Jörg J Goronzy

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
301citing papers in PubMed, 3 pooled it
7.8field-weighted citation impact, top 2% 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

301 citing papers in PubMed, 3 syntheses or guidelines pooled it, 532 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. [Clinical characteristics and risk factors of patients with rheumatoid arthritis complicated with urinary tract infection].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
    Article
  9. Observational
  10. Article
  11. Review
  12. Article
  13. Risk Factors for Secondary Immunodeficiency in the Aged.The journal of allergy and clinical immunology. In practice · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Observational
  20. Article

241 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Cornelia M WeyandDepartment of Medicine, Stanford University Medical School, Stanford, California.
Jörg J GoronzyDepartment of Medicine, Stanford University Medical School, Stanford, California.
Stanford University · US

Funding

Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI HARRISON, DAVID G · 1998 to 2013
$20.7M
The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2016 to 2020
$12.4M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
microRNA Regulation of T Cell SenescenceR01AI108891 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2014 to 2023
$4.6M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
Influence of Age on CD4 T Memory CellsR01AG045779 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2013 to 2023
$4.0M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
T Cell Signaling in Rheumatoid ArthritisI01BX001669 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI GORONZY, JORG J · 2012 to 2021
–
BLRD VA I01 BX001669NHLBI NIH HHS P01 HL058000NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL117913NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

Beginning with the sixth decade of life, the human immune system undergoes dramatic aging-related changes, which continuously progress to a state of immunosenescence. The aging immune system loses the ability to protect against infections and cancer and fails to support appropriate wound healing. Vaccine responses are typically impaired in older individuals. Conversely, inflammatory responses mediated by the innate immune system gain in intensity and duration, rendering older individuals susceptible to tissue-damaging immunity and inflammatory disease. Immune system aging functions as an accelerator for other age-related pathologies. It occurs prematurely in some clinical conditions, most prominently in patients with the autoimmune syndrome rheumatoid arthritis (RA); and such patients serve as an informative model system to study molecular mechanisms of immune aging. T cells from patients with RA are prone to differentiate into proinflammatory effector cells, sustaining chronic-persistent inflammatory lesions in the joints and many other organ systems. RA T cells have several hallmarks of cellular aging; most importantly, they accumulate damaged DNA. Because of deficiency of the DNA repair kinase ataxia telangiectasia mutated, RA T cells carry a higher burden of DNA double-strand breaks, triggering cell-indigenous stress signals that shift the cell's survival potential and differentiation pattern. Immune aging in RA T cells is also associated with metabolic reprogramming; specifically, with reduced glycolytic flux and diminished ATP production. Chronic energy stress affects the longevity and the functional differentiation of older T cells. Altered metabolic patterns provide opportunities to therapeutically target the immune aging process through metabolic interference.

Indexed as

AgingArthritis, RheumatoidAtaxia Telangiectasia Mutated ProteinsCell SurvivalCellular SenescenceDNA DamageDNA RepairHumansImmune SystemImmunosenescenceInflammationT-LymphocytesAtaxia Telangiectasia Mutated ProteinsDNA damageglycolysisimmune aginginflammationT cells

Identifiers

PMID28005419
PMCPMC5291468
OpenAlexW2562443541

What OpenQuestion holds

Textmetadata
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.