Evidence map›Paper›PMID 24684878›Full record

ReviewMayo Clinic proceedings2014

Targets of immune regeneration in rheumatoid arthritis.

Philipp J Hohensinner, Jörg J Goronzy, Cornelia M Weyand

Open access · bronzeAbstract readReview
In one paragraph

Review in Mayo Clinic proceedings, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Bcl2 like protein-12 suppresses Foxp3American journal of translational research · 2019
    Article
  5. Article
  6. Article
  7. Aging of the Immune System. Mechanisms and Therapeutic Targets.Annals of the American Thoracic Society · 2016
    Review
  8. Article
  9. GHK and DNA: resetting the human genome to health.BioMed research international · 2014
    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.

Philipp J HohensinnerDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA.
Jörg J GoronzyDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA.
Cornelia M WeyandDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA. Electronic address: cweyand@stanford.edu.
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
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
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
T CELLS AND AGINGR01AG015043 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 1998 to 2008
$2.1M
CD8 T cells in Rheumatoid ArthritisR56AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2013 to 2013
$369k
NHLBI NIH HHS P01 HL058000NHLBI NIH HHS R01 HL117913NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI08906NIAID NIH HHS R01 AI108906NIAID NIH HHS R56 AI044142NIAID NIH HHS U19 AI057266NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG015043
6 · The paper itself

Abstract

Many of the aging-related morbidities, including cancer, cardiovascular disease, neurodegenerative disease, and infectious susceptibility, are linked to a decline in immune competence with a concomitant rise in proinflammatory immunity, placing the process of immune aging at the center of aging biology. Immune aging affects individuals older than 50 years and is accelerated in patients with the autoimmune disease rheumatoid arthritis. Immune aging results in a marked decline in protective immune responses and a parallel increase in tissue inflammatory responses. By studying immune cells in patients with rheumatoid arthritis, several of the molecular underpinnings of the immune aging process have been delineated, such as the loss of telomeres and inefficiencies in the repair of damaged DNA. Aging T cells display a series of abnormalities, including the unopposed up-regulation of cytoplasmic phosphatases and the loss of glycolytic competence, that alter their response to stimulating signals and undermine their longevity. Understanding the connection between accelerated immune aging and autoimmunity remains an area of active research. With increasing knowledge of the molecular pathways that cause immunosenescence, therapeutic interventions can be designed to slow or halt the seemingly inevitable deterioration of protective immunity with aging.

Indexed as

AgedAgingArthritis, RheumatoidAutoimmune DiseasesCellular SenescenceDisease ProgressionDNA DamageDNA RepairFemaleHumansMaleMiddle AgedRegenerationSensitivity and SpecificityT-Lymphocytes

Identifiers

PMID24684878
PMCPMC4605139
OpenAlexW2125313585

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.