Evidence map›Paper›PMID 33257900›Full record

ReviewNature immunology2021

The immunology of rheumatoid arthritis.

Cornelia M Weyand, Jörg J Goronzy

Open access · greenAbstract readReview
In one paragraph

Review in Nature immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 451 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
451citing papers in PubMed, 2 pooled it
28.6field-weighted citation impact, top 1% 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

451 citing papers in PubMed, 2 syntheses or guidelines pooled it, 752 citations in OpenAlex.

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391 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 School of Medicine, Stanford, CA, USA. cweyand@stanford.edu.ORCID http://orcid.org/0000-0003-2230-9802
Jörg J GoronzyDepartment of Medicine, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-7670-1856
VA Palo Alto Health Care System · US

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
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
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
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
T Cell Immunity in Giant Cell ArteritisR01HL142068 · NHLBI · STANFORD UNIVERSITY · PI Cornelia M. Weyand · 2018 to 2026
$3.3M
Memory T Cell Development and Survival in T Cell Responses of Older IndividualsR01AI129191 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2017 to 2021
$1.9M
T Cell Signaling in Rheumatoid ArthritisI01BX001669 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI GORONZY, JORG J · 2012 to 2021
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BLRD VA I01 BX001669NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL117913NHLBI NIH HHS R01 HL142068NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIAID NIH HHS R01 AI129191NIAID NIH HHS U19 AI057266NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

The immunopathogenesis of rheumatoid arthritis (RA) spans decades, beginning with the production of autoantibodies against post-translationally modified proteins (checkpoint 1). After years of asymptomatic autoimmunity and progressive immune system remodeling, tissue tolerance erodes and joint inflammation ensues as tissue-invasive effector T cells emerge and protective joint-resident macrophages fail (checkpoint 2). The transition of synovial stromal cells into autoaggressive effector cells converts synovitis from acute to chronic destructive (checkpoint 3). The loss of T cell tolerance derives from defective DNA repair, causing abnormal cell cycle dynamics, telomere fragility and instability of mitochondrial DNA. Mitochondrial and lysosomal anomalies culminate in the generation of short-lived tissue-invasive effector T cells. This differentiation defect builds on a metabolic platform that shunts glucose away from energy generation toward the cell building and motility programs. The next frontier in RA is the development of curative interventions, for example, reprogramming T cell defects during the period of asymptomatic autoimmunity.

Indexed as

AnimalsArthritis, RheumatoidAutoimmunityDNA RepairHumansInflammationSelf ToleranceSynovitisT-Lymphocytes

Identifiers

PMID33257900
PMCPMC8557973
OpenAlexW3109820229

What Socratic 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 Socratic graph.