Evidence map›Paper›PMID 35729334›Full record

ReviewNature reviews. Rheumatology2022

IL-1 and autoinflammatory disease: biology, pathogenesis and therapeutic targeting.

Lori Broderick, Hal M Hoffman

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

Review in Nature reviews. Rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 88 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 5 pooled it
12.5field-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

88 citing papers in PubMed, 5 syntheses or guidelines pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Review
  8. Article
  9. Association of Interleukin 1 Receptor Antagonist (International journal of molecular sciences · 2026
    Article
  10. Review
  11. Biologics for cardiovascular diseases: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Food science & nutrition · 2026
    Article
  16. Article
  17. Article
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  20. Proceedings of the 2Mediterranean journal of rheumatology · 2026
    Article

28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Lori BroderickDivision of Allergy, Immunology & Rheumatology, Department of Paediatrics, University of California, San Diego, CA, USA. lbroderick@health.ucsd.edu.ORCID http://orcid.org/0000-0001-6147-7097
Hal M HoffmanDivision of Allergy, Immunology & Rheumatology, Department of Paediatrics, University of California, San Diego, CA, USA. hahoffman@health.ucsd.edu.ORCID http://orcid.org/0000-0001-8609-2548
University of California San Diego · US

Funding

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
NHLBI NIH HHS R01 HL140898NIDDK NIH HHS R01 DK113592
6 · The paper itself

Abstract

Over 20 years ago, it was first proposed that autoinflammation underpins a handful of rare monogenic disorders characterized by recurrent fever and systemic inflammation. The subsequent identification of novel, causative genes directly led to a better understanding of how the innate immune system is regulated under normal conditions, as well as its dysregulation associated with pathogenic mutations. Early on, IL-1 emerged as a central mediator for these diseases, based on data derived from patient cells, mutant mouse models and definitive clinical responses to IL-1 targeted therapy. Since that time, our understanding of the mechanisms of autoinflammation has expanded beyond IL-1 to additional innate immune processes. However, the number and complexity of IL-1-mediated autoinflammatory diseases has also multiplied to include additional monogenic syndromes with expanded genotypes and phenotypes, as well as more common polygenic disorders seen frequently by the practising clinician. In order to increase physician awareness and update rheumatologists who are likely to encounter these patients, this review discusses the general pathophysiological concepts of IL-1-mediated autoinflammation, the epidemiological and clinical features of specific diseases, diagnostic challenges and approaches, and current and future perspectives for therapy.

Indexed as

Hereditary Autoinflammatory DiseasesAnimalsBiologyHumansInflammationInterleukin-1MiceInterleukin-1

Identifiers

PMID35729334
PMCPMC9210802
OpenAlexW4283271499

What OpenQuestion holds

Textmetadata
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.