Evidence map›Paper›PMID 32477606›Full record

ArticleImmunometabolism2020

Metabolic Fitness of T Cells in Autoimmune Disease.

Bowen Wu, Jörg J Goronzy, Cornelia M Weyand

Open access · diamondAbstract read
In one paragraph

Article in Immunometabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Immune Aging in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Effects of Aging on Metabolic Characteristics of Human B Cells.Journal of acquired immune deficiency syndromes (1999) · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Mechanism of miR-218-5p in autophagy, apoptosis and oxidative stress in rheumatoid arthritis synovial fibroblasts is mediated by KLF9 and JAK/STAT3 pathways.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2021
    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 2 institutions in 1 country.

Bowen WuSchool of Medicine, Stanford University, Stanford, CA 94305, USA.
Jörg J GoronzySchool of Medicine, Stanford University, Stanford, CA 94305, USA.
Cornelia M WeyandSchool of Medicine, Stanford University, Stanford, CA 94305, USA.
Stanford University · USVA 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
Systems Biological Analysis of Innate and Adaptive Responses to VaccinationU19AI090023 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI, LI, SHUZHAO · 2010 to 2021
$45.0M
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
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 AI057266NIAID NIH HHS U19 AI090023NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are relatively common autoimmune diseases, often considered prototypic examples for how protective immunity switches to destructive immunity. The autoantigens recognized in RA and SLE are distinct, clinical manifestations are partially overlapping. A shared feature is the propensity of the adaptive immune system to respond inappropriately, with T cell hyper-responsiveness a pinnacle pathogenic defect. Upon antigen recognition, T cells mobilize a multi-pranged metabolic program, enabling them to massively expand and turn into highly mobile effector cells. Current evidence supports that T cells from patients with RA or SLE adopt metabolic programs different from healthy T cells, in line with the concept that autoimmune effector functions rely on specified pathways of energy sensing, energy generation and energy utilization. Due to misrouting of the energy sensor AMPK, RA T cells have a defect in balancing catabolic and anabolic processes and deviate towards a cell-building program. They supply biosynthetic precursors by shunting glucose away from glycolytic breakdown towards the pentose phosphate pathway and upregulate lipogenesis, enabling cellular motility and tissue invasiveness. Conversely, T cells from SLE patients are committed to high glycolytic flux, overusing the mitochondrial machinery and imposing oxidative stress. Typically, disease-relevant effector functions in SLE are associated with inappropriate activation of the key metabolic regulator mTORC1. Taken together, disease-specific metabolic signatures in RA and SLE represent vulnerabilities that are therapeutically targetable to suppress pathogenic immune responses.

Indexed as

glucoseglycolysislipid dropletslipogenesismitochondriaoxygen consumptionrheumatoid arthritissystemic lupus erythematosusT cells

Identifiers

PMID32477606
PMCPMC7261019
OpenAlexW3017707604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.