Evidence map›Paper›PMID 26385789›Full record

ArticleArthritis research & therapy2015

Enhanced activity of NLRP3 inflammasome in peripheral blood cells of patients with active rheumatoid arthritis.

Christianna Choulaki, Garyfallia Papadaki, Argyro Repa, Eleni Kampouraki, Konstantinos Kambas, Konstantinos Ritis, George Bertsias, Dimitrios T Boumpas, Prodromos Sidiropoulos

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Microparticles synthesized from itaconate polyesters enable metabolite delivery and elicit immunoregulatory outcomes.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  3. A novel small molecule KMU-11361 attenuates rheumatoid arthritis by mechanistic inhibition of the TAK1-NF-κB-NLRP3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Synthesis, characterization andNanoscale advances · 2025
    Article
  11. Article
  12. ACPA-Induced ATP release and KCell communication and signaling : CCS · 2025
    Article
  13. NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024
    Review
  20. Review

42 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

9 authors at 3 institutions in 2 countries.

Christianna ChoulakiRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. choulaki@med.uoc.gr.
Garyfallia PapadakiRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. litsapap85@yahoo.com.
Argyro RepaRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. arrepa2002@yahoo.gr.
Eleni KampourakiRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. elenkabouraki@yahoo.gr.
Konstantinos KambasLaboratory of Molecular Hematology, Democritus University of Thrace, 68100, Alexandroupolis, Greece. kkampas@hotmail.com.
Konstantinos RitisLaboratory of Molecular Hematology, Democritus University of Thrace, 68100, Alexandroupolis, Greece. kritis@med.duth.gr.
George BertsiasRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. gbert@med.uoc.gr.
Dimitrios T BoumpasDivision of Infections and Immunity, Institute of Molecular Biology and Biotechnology-FORTH, Nikolaou Plastira 100, 70013, Iraklion, Greece. boumpasd@med.uoc.gr.
Prodromos SidiropoulosRheumatology, Clinical Immunology and Allergy, Faculty of Medicine, University of Crete, 71003, Iraklion, Greece. sidiropp@med.uoc.gr.
University of Crete · GRDemocritus University of Thrace · GRNational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionInterleukin-1β (IL-1β) is a major inflammatory cytokine, produced predominantly by innate immune cells through NLRP3-inflammasome activation. Both intrinsic and extrinsic danger signals may activate NLRP3. Genetic variations in NLRP3-inflammasome components have been reported to influence rheumatoid arthritis (RA) susceptibility and severity. We sought to assess the activity of NLRP3-inflammasome in patients with active RA compared to healthy individuals.

methodIntracellular protein expression of NLRP3, ASC, pro- and active caspase-1, pro- and active IL-1β was assessed by immunoblotting both at baseline and upon inflammasome activation. NLRP3 function (IL-1β secretion) was assessed upon priming of TLR2 (Pam(3)CysSK(4), TLR3 (poly(I:C)) or TLR4 (LPS) and ATP sequential treatment. We used caspase inhibitors (casp-1, 3/7 and 8) to assess their contribution to IL-1β maturation. All experiments were performed in whole blood cells.

resultsActive RA patients (n = 11) expressed higher basal intracellular levels of NLRP3 (p < 0.008), ASC (p < 0.003), active caspase-1 (p < 0.02) and pro-IL-1β (p < 0.001). Upon priming with TLR4 (LPS) and ATP, RA-derived cell extracts (n = 7) displayed increased expression of NLRP3 (p < 0.01) and active caspase-1 (p < 0.001). Secreted IL-1β in culture supernatants from whole blood cells activated with TLR4 (LPS) or TLR3 agonist (poly(I:C)) plus ATP was higher in RA patients (n = 20) versus controls (n = 18) (p < 0.02 for both). Caspase-1 inhibition significantly reduced IL-1β secretion induced by all stimuli, whereas caspase-8 inhibition affected only TLR4 and TLR3 cell priming.

conclusionPatients with active RA have increased expression of NLRP3 and NLRP3-mediated IL-1β secretion in whole blood cells upon stimulation via TLR3 and TLR4 but not TLR2. In these patients, IL-1β secretion seems to be predominately driven by caspase-1 and caspase-8. Targeting NLRP3 or downstream caspases may be of benefit in suppressing IL-1β production in RA.

Indexed as

Arthritis, RheumatoidBlotting, WesternCarrier ProteinsEnzyme-Linked Immunosorbent AssayFemaleHumansInflammasomesLeukocytesMaleMiddle AgedNLR Family, Pyrin Domain-Containing 3 ProteinCarrier ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID26385789
PMCPMC4575443
OpenAlexW1942500899

What OpenQuestion holds

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LicenceCC BY
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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.