Evidence map›Paper›PMID 38146057›Full record

ReviewImmunological reviews2024

The discovery of NLRP3 and its function in cryopyrin-associated periodic syndromes and innate immunity.

Christopher D Putnam, Lori Broderick, Hal M Hoffman

Open access · hybridAbstract readReview
In one paragraph

Review in Immunological reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Review
  3. Fibroblasts resistScience advances · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Mechanistic insights into natural product-driven modulation of NLRP3-inflammasome signalling in metabolic syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Gout and NLRP3 Inflammasome Biology.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. p16Journal of cardiovascular translational research · 2025
    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.

Christopher D PutnamDepartment of Medicine, University of California, San Diego, La Jolla, California, USA.ORCID 0000-0002-6145-1265
Lori BroderickDivision of Allergy, Immunology & Rheumatology, Department of Pediatrics, University of California, San Diego, La Jolla, California, USA.ORCID 0000-0001-6147-7097
Hal M HoffmanDepartment of Medicine, University of California, San Diego, La Jolla, California, USA.ORCID 0000-0001-8609-2548
La Jolla Institute for Immunology · USUniversity of California San Diego · US

Funding

Neutrophil Survival and Demise During Inflammatory StatesP01HL152958 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI HOFFMAN, HAROLD M · 2021 to 2025
$12.4M
Vesicular trafficking mechanisms regulating granulocyte functionR01HL088256 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI Sergio Daniel Catz · 2009 to 2026
$9.0M
Sterile inflammation and pyroptotic cell death in liver fibrosisR01DK113592 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ariel Feldstein, HAROLD M HOFFMAN · 2017 to 2026
$4.8M
Innate Immune Activation and Endothelial Cell Dysfunction in Acute Kawasaki DiseaseR01HL140898 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BURNS, JANE C, HOFFMAN, HAROLD M · 2018 to 2022
$4.3M
The Neutrophil Lineage in InflammasomopathiesR01AI155869 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CROKER, BEN ADAM, HOFFMAN, HAROLD M · 2020 to 2024
$2.0M
NHLBI NIH HHS P01 HL152958NHLBI NIH HHS R01 HL088256NHLBI NIH HHS R01 HL140898NIAID NIH HHS R01 AI155869NIDDK NIH HHS R01 DK113592NIH HHS P01HL152958NIH HHS R01AI155869NIH HHS R01DK113592NIH HHS R01HL140898
6 · The paper itself

Abstract

From studies of individual families to global collaborative efforts, the NLRP3 inflammasome is now recognized to be a key regulator of innate immunity. Activated by a panoply of pathogen-associated and endogenous triggers, NLRP3 serves as an intracellular sensor that drives carefully coordinated assembly of the inflammasome, and downstream inflammation mediated by IL-1 and IL-18. Initially discovered as the cause of the autoinflammatory spectrum of cryopyrin-associated periodic syndrome (CAPS), NLRP3 is now also known to play a role in more common diseases including cardiovascular disease, gout, and liver disease. We have seen cohesion in results from clinical studies in CAPS patients, ex vivo studies of human cells and murine cells, and in vivo murine models leading to our understanding of the downstream pathways, cytokine secretion, and cell death pathways that has solidified the role of autoinflammation in the pathogenesis of human disease. Recent advances in our understanding of the structure of the inflammasome have provided ways for us to visualize normal and mutant protein function and pharmacologic inhibition. The subsequent development of targeted therapies successfully used in the treatment of patients with CAPS completes the bench to bedside translational loop which has defined the study of this unique protein.

Indexed as

Cryopyrin-Associated Periodic SyndromesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsHumansImmunity, InnateInflammasomesInflammationInterleukin-1betaMiceInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 Proteincryopyrin-associated periodic syndromefamilial cold autoinflammatory syndromeinflammasomeNLRP3

Identifiers

PMID38146057
PMCPMC10950545
OpenAlexW4390234972

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.