Evidence map›Paper›PMID 40018678›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2025

Development of anti-murine IL-18 binding protein antibodies to stimulate IL-18 bioactivity.

Arnaud Huard, Sébastien Fauteux-Daniel, Jérémie Goldstein, Praxedis Martin, Matthias Jarlborg, Julie Andries, Assunta Caruso, Alejandro Díaz-Barreiro, Emiliana Rodriguez, Laurie Vaillant and 2 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Arnaud HuardDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Sébastien Fauteux-DanielDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Jérémie GoldsteinDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Praxedis MartinDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Matthias JarlborgDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Julie AndriesDepartment of Biochemistry and Microbiology, Ghent University, 9052, Ghent, Belgium.
Assunta CarusoDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Alejandro Díaz-BarreiroDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Emiliana RodriguezDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Laurie VaillantDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Savvas N SavvidesDepartment of Biochemistry and Microbiology, Ghent University, 9052, Ghent, Belgium.
Cem GabayDivision of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-18 is an immunoregulatory cytokine that acts as a potent inducer of T helper 1 and cytotoxic responses. IL-18 activity is regulated by its decoy receptor IL-18 binding protein (IL-18BP) which forms a high affinity complex with IL-18 to block binding of the cognate receptors. A disbalance between IL-18 and IL-18BP associated with excessive IL-18 signaling can lead to systemic inflammation. Indeed, the severity of CpG-induced macrophage activation syndrome (MAS) is exacerbated in IL-18BP KO mice. On the contrary, targeting IL-18BP can have promising effects to enhance immune responses against pathogens and cancer. We generated monoclonal rabbit anti-mouse IL-18BP antibodies labeled from 441 to 450. All antibodies, except from antibody 443, captured mIL-18BP when used in a sandwich ELISA. Using an IL-18 bioassay, we showed that antibody 441 did not interfere with the regulatory effect of mIL-18BP, whereas all other antibodies displayed different levels of antagonism. Further experiments were performed using antibody 445 endowed with potent neutralizing activity and antibody 441. Despite binding to IL-18BP with the same affinity, antibody 445, but not antibody 441, was able to release IL-18 from preformed IL-18-IL-18BP complexes. Administration of antibody 445 significantly aggravated the severity of CpG-induced MAS as compared to antibody 441. Additional experiments using naïve WT, IL-18BP KO, and IL-18 KO mice confirmed the specificity of the neutralizing effect of antibody 445 towards IL-18BP. Our studies led to the development of a monoclonal anti-IL-18BP antibody with neutralizing activity that results in the promotion of IL-18 activities.

Indexed as

Antibodies, MonoclonalIntercellular Signaling Peptides and ProteinsInterleukin-18AnimalsHumansMiceMice, Inbred C57BLMice, KnockoutAntibodies, MonoclonalIntercellular Signaling Peptides and ProteinsInterleukin-18interleukin-18 binding proteinIL-18 binding proteinInterleukin (IL)-18macrophage activation syndromemonoclonal antibodies

Identifiers

PMID40018678
PMCPMC7617445

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Registered trials

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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.