Evidence map›Paper›PMID 24422572›Full record

ReviewAnnual review of medicine2014

IL-1 blockade in autoinflammatory syndromes.

Adriana A Jesus, Raphaela Goldbach-Mansky

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Annual review of medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 5 pooled it
15.5field-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

159 citing papers in PubMed, 5 syntheses or guidelines pooled it, 325 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Cell stress increases ATP release in NLRP3 inflammasome-mediated autoinflammatory diseases, resulting in cytokine imbalance.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Trial
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Nature-inspired IL-1 targeted therapy to treat chronic inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

99 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 2 countries.

Adriana A JesusTranslational Autoinflammatory Disease Section, National Institute of Arthritis, Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health, Bethesda, Maryland 20982; email: goldbacr@mail.nih.gov.
Raphaela Goldbach-Mansky
National Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

Pathogenesis and treatment studies in patients with NOMID and related diseasesZIAAR041138 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GOLDBACH-MANSKY, RAPHAELA · 2009 to 2016
$8.6M
Intramural NIH HHS ZIA AR041138
6 · The paper itself

Abstract

Monogenic autoinflammatory syndromes present with excessive systemic inflammation including fever, rashes, arthritis, and organ-specific inflammation and are caused by defects in single genes encoding proteins that regulate innate inflammatory pathways. Pathogenic variants in two interleukin-1 (IL-1)-regulating genes, NLRP3 and IL1RN, cause two severe and early-onset autoinflammatory syndromes, CAPS (cryopyrin associated periodic syndromes) and DIRA (deficiency of IL-1 receptor antagonist). The discovery of the mutations that cause CAPS and DIRA led to clinical and basic research that uncovered the key role of IL-1 in an extended spectrum of immune dysregulatory conditions. NLRP3 encodes cryopyrin, an intracellular "molecular sensor" that forms a multimolecular platform, the NLRP3 inflammasome, which links "danger recognition" to the activation of the proinflammatory cytokine IL-1β. The success and safety profile of drugs targeting IL -1 in the treatment of CAPS and DIRA have encouraged their wider use in other autoinflammatory syndromes including the classic hereditary periodic fever syndromes (familial Mediterranean fever, TNF receptor-associated periodic syndrome, and hyperimmunoglobulinemia D with periodic fever syndrome) and additional immune dysregulatory conditions that are not genetically well defined, including Still's, Behcet's, and Schnitzler diseases. The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1β-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsCarrier ProteinsHereditary Autoinflammatory DiseasesHumansInflammasomesInterleukin-1Interleukin 1 Receptor Antagonist ProteinNLR Family, Pyrin Domain-Containing 3 ProteinRecombinant Fusion ProteinsSignal TransductionAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentscanakinumabCarrier ProteinsIL1RN protein, humanInflammasomesInterleukin-1Interleukin 1 Receptor Antagonist ProteinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanRecombinant Fusion Proteinsrilonacept

Identifiers

PMID24422572
PMCPMC4178953
OpenAlexW2163337422

What OpenQuestion 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 OpenQuestion graph.