Evidence map›Paper›PMID 38636519›Full record

ArticleCell reports2024

Antibodies targeting the shared cytokine receptor IL-1 receptor accessory protein invoke distinct mechanisms to block all cytokine signaling.

James K Fields, Elin Jaensson Gyllenbäck, Marek Bogacz, Juliet Obi, Gabriel Svensson Birkedal, Kjell Sjöström, Kino Maravillas, Caitríona Grönberg, Sara Rattik, Kyle Kihn and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

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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

18 authors at 3 institutions in 2 countries.

James K FieldsDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA; Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.
Elin Jaensson GyllenbäckCantargia AB, Lund, Sweden.
Marek BogaczDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
Juliet ObiDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.
Gabriel Svensson BirkedalCantargia AB, Lund, Sweden.
Kjell SjöströmInnovagen AB, Lund, Sweden.
Kino MaravillasDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
Caitríona GrönbergCantargia AB, Lund, Sweden.
Sara RattikCantargia AB, Lund, Sweden.
Kyle KihnDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.
Maria FlowersDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
Ally K SmithDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.
Nils HansenDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Thoas FioretosDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Chau HuyhnDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
David LibergCantargia AB, Lund, Sweden.
Daniel DeredgeDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.
Eric J SundbergDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA. Electronic address: eric.sundberg@emory.edu.
Emory University · USUniversity of Maryland, Baltimore · USLund University · SE

Funding

Molecular mechanisms of IL-33 cytokine signalingR01AI132766 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI SUNDBERG, ERIC JOHN · 2017 to 2021
$2.5M
NIAID NIH HHS R01 AI132766
6 · The paper itself

Abstract

Interleukin-1 (IL-1)-family cytokines are potent modulators of inflammation, coordinating a vast array of immunological responses across innate and adaptive immune systems. Dysregulated IL-1-family cytokine signaling, however, is involved in a multitude of adverse health effects, such as chronic inflammatory conditions, autoimmune diseases, and cancer. Within the IL-1 family of cytokines, six-IL-1α, IL-1β, IL-33, IL-36α, IL-36β, and IL-36γ-require the IL-1 receptor accessory protein (IL-1RAcP) as their shared co-receptor. Common features of cytokine signaling include redundancy of signaling pathways, sharing of cytokines and receptors, pleiotropy of the cytokines themselves, and multifaceted immune responses. Accordingly, targeting multiple cytokines simultaneously is an emerging therapeutic strategy and can provide advantages over targeting a single cytokine pathway. Here, we show that two monoclonal antibodies, CAN10 and 3G5, which target IL-1RAcP for broad blockade of all associated cytokines, do so through distinct mechanisms and provide therapeutic opportunities for the treatment of inflammatory diseases.

Indexed as

CytokinesInterleukin-1 Receptor Accessory ProteinSignal TransductionAnimalsAntibodies, MonoclonalHumansInflammationMiceAntibodies, MonoclonalCytokinesInterleukin-1 Receptor Accessory Protein3G5antibodyCAN10CP: ImmunologycytokineIL-1IL-33IL-36shared receptorsignaling inhibition

Identifiers

PMID38636519
PMCPMC11587196
OpenAlexW4394893750

What Socratic 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 Socratic graph.