Evidence map›Paper›PMID 26209330›Full record

ReviewRheumatology (Oxford, England)2015

Treating rheumatological diseases and co-morbidities with interleukin-1 blocking therapies.

Giulio Cavalli, Charles A Dinarello

Abstract readReview
In one paragraph

Review in Rheumatology (Oxford, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

97 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Immune gene correlation networks differentiate both chronic lung allograft dysfunction and survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
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  17. The IL-1 Family and Its Role in Atherosclerosis.International journal of molecular sciences · 2022
    Review
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  19. Article
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37 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.

Giulio CavalliDepartment of Medicine, University of Colorado Denver, Aurora, CO, USA, Division of Internal Medicine and Clinical Immunology, IRCCS San Raffaele Scientific Institute, Milan, Italy and cavalli.giulio@gmail.com.
Charles A DinarelloDepartment of Medicine, University of Colorado Denver, Aurora, CO, USA, Department of Internal Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands.

Funding

Yeast-based HTS Assay Technologies for ProteasesR01AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1985 to 2025
$8.5M
VitiligoR01AR045584 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 1999 to 2014
$6.2M
Pathogenesis of Fever in ManR56AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 2016 to 2016
$311k
PATHOGENESIS OF FEVER IN HUMANSR37AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1988 to 1998
–
NIAID NIH HHS AI-15614NIAID NIH HHS R01 AI015614NIAID NIH HHS R56 AI015614NIAMS NIH HHS AR-45584NIAMS NIH HHS R01 AR045584
6 · The paper itself

Abstract

The inflammatory cytokines IL-1α and IL-1β orchestrate local and systemic inflammatory responses underlying a broad spectrum of diseases. Three agents for reducing IL-1 activities are currently available. Anakinra is a recombinant form of the naturally occurring IL-1 receptor antagonist. Anakinra binds to the IL-1 receptor and prevents the activity of IL-1α and IL-1β. The soluble decoy receptor rilonacept and the neutralizing mAb canakinumab block IL-1β. A mAb directed against the IL-1 receptor and a neutralizing anti-human IL-1α are in clinical trials. The availability of therapies specifically targeting IL-1 unveiled the pathological role of IL-1-mediated inflammation in a broadening list of diseases. Conditions effectively treated with agents blocking IL-1 range from classic rheumatic diseases, such as RA and gout, to autoinflammatory syndromes, such as systemic JIA and FMF. However, IL-1 antagonism is also effective against highly prevalent inflammatory diseases, namely cardiovascular diseases and type 2 diabetes, conditions that are frequently encountered as co-morbidities in patients with rheumatic diseases. Thereby, IL-1 inhibition has the potential to lift the burden of disease for patients with rheumatic conditions, but also to provide clinical benefits beyond the efficacy on osteoarticular manifestations.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsAutoimmune DiseasesComorbidityHereditary Autoinflammatory DiseasesHumansInterleukin-1Receptors, Interleukin-1Recombinant Fusion ProteinsRheumatic DiseasesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentscanakinumabInterleukin-1Receptors, Interleukin-1Recombinant Fusion Proteinsrilonaceptanakinraautoinflammatory syndromescanakinumabcardiovascular diseasediabetesIL-1αIL-1βinterleukin-1rheumatoid arthritis

Identifiers

PMID26209330
PMCPMC5009422

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.