Evidence map›Paper›PMID 28841779›Full record

ReviewArthritis & rheumatology (Hoboken, N.J.)2017

Review: Metabolic Control of Immune System Activation in Rheumatic Diseases.

Andras Perl

Open access · hybridAbstract readReview
In one paragraph

Review in Arthritis & rheumatology (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
9.7field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Immune responses in aging adults.The Journal of clinical investigation · 2026
    Review
  6. Review
  7. Review
  8. Cellular Metabolic Disorders in a Cohort of Patients with Sjogren's Disease.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024
    Review
  19. Article
  20. Article

12 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

1 author at 1 institution in 1 country.

Andras PerlState University of New York, Upstate Medical University, Syracuse.
SUNY Upstate Medical University · US

Funding

Metabolic Control of T-cell Lineage Specification in SLER01AI072648 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2024
$6.1M
IMPACT OF HRES-1 ENDOGENOUS RETROVIRUS IN SLER01AI048079 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2000 to 2013
$2.7M
Endocytic Control of Autophagosome Formation in Lupus T cellsR01AI122176 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2016 to 2020
$2.0M
Pathogenesis and Treatment of Liver Disease in Transaldolase DeficiencyR01DK078922 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2010 to 2013
$1.4M
Treatment of Systemic Lupus Erythematosus (SLE) with N-acetylcysteine (NAC)R34AR068052 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI MCDERMOTT, MICHAEL P, PERL, ANDRAS · 2016 to 2017
$405k
Mitochondrial dysfunction in patients with SLER21AI061066 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2004 to 2004
$266k
NIAID NIH HHS R01 AI048079NIAID NIH HHS R01 AI072648NIAID NIH HHS R01 AI122176NIAID NIH HHS R21 AI061066NIAMS NIH HHS R34 AR068052NIDDK NIH HHS R01 DK078922
6 · The paper itself

Abstract

Metabolic pathways mediate lineage specification within the immune system through the regulation of glucose utilization, a process that generates energy in the form of ATP and synthesis of amino acids, nucleotides, and lipids to enable cell growth, proliferation, and survival. CD4+ T cells, a proinflammatory cell subset, preferentially produce ATP through glycolysis, whereas cells with an antiinflammatory lineage, such as memory and regulatory T cells, favor mitochondrial ATP generation. In conditions of metabolic stress or a shortage of nutrients, cells rely on autophagy to secure amino acids and other substrates, while survival depends on the sparing of mitochondria and maintenance of a reducing environment. The pentose phosphate pathway acts as a key gatekeeper of inflammation by supplying ribose-5-phosphate for cell proliferation and NADPH for antioxidant defenses. Increased lysosomal catabolism, accumulation of branched amino acids, glutamine, kynurenine, and histidine, and depletion of glutathione and cysteine activate the mechanistic target of rapamycin (mTOR), an arbiter of lineage development within the innate and adaptive immune systems. Mapping the impact of susceptibility genes to metabolic pathways allows for better understanding and therapeutic targeting of disease-specific expansion of proinflammatory cells. Therapeutic approaches aimed at glutathione depletion and mTOR pathway activation appear to be safe and effective for treating lupus, while an opposing intervention may be of benefit in rheumatoid arthritis. Environmental sources of origin for metabolites within immune cells may include microbiota and plants. Thus, a better understanding of the pathways of immunometabolism could provide new insights into the pathogenesis and treatment of the rheumatic diseases.

Indexed as

GlucoseGlutathioneGlycolysisHumansImmune SystemMetabolic Networks and PathwaysRheumatic DiseasesTOR Serine-Threonine KinasesGlucoseGlutathioneMTOR protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID28841779
PMCPMC5711528
OpenAlexW2745824965

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.