Evidence map›Paper›PMID 39374239›Full record

ArticlePloS one2024

Targeting of oxidized Macrophage Migration Inhibitory Factor (oxMIF) with antibody ON104 attenuates the severity of glomerulonephritis.

Maroua Ferhat, Julia Mayer, Lyndon H Costa, Maria Prendecki, Alejandro A Puchol Tarazona, Alexander Schinagl, Randolf J Kerschbaumer, Frederick W K Tam, Christine Landlinger, Michael Thiele

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Maroua FerhatOncoOne Research & Development GmbH, Vienna, Austria.ORCID 0000-0002-1298-4620
Julia MayerOncoOne Research & Development GmbH, Vienna, Austria.
Lyndon H CostaDepartment of Immunology and Inflammation, Centre for Inflammatory Disease, Hammersmith Hospital, Imperial College London (ICL), London, United Kingdom.
Maria PrendeckiDepartment of Immunology and Inflammation, Centre for Inflammatory Disease, Hammersmith Hospital, Imperial College London (ICL), London, United Kingdom.
Alejandro A Puchol TarazonaOncoOne Research & Development GmbH, Vienna, Austria.
Alexander SchinaglOncoOne Research & Development GmbH, Vienna, Austria.ORCID 0000-0002-6060-969X
Randolf J KerschbaumerOncoOne Research & Development GmbH, Vienna, Austria.
Frederick W K TamDepartment of Immunology and Inflammation, Centre for Inflammatory Disease, Hammersmith Hospital, Imperial College London (ICL), London, United Kingdom.
Christine LandlingerOncoOne Research & Development GmbH, Vienna, Austria.
Michael ThieleOncoOne Research & Development GmbH, Vienna, Austria.ORCID 0000-0002-3003-9999

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oxidized form of Macrophage Migration Inhibitory Factor (oxMIF) has been identified as the disease-related isoform of MIF, exerting pathological functions in inflamed tissue. In this study, we aimed to explore the in vivo effects of the neutralizing anti-oxMIF antibody ON104 in a rat model of crescentic glomerulonephritis (CGN), to better understand its disease modifying activities. WKY rats received a single intravenous injection of a rabbit nephrotoxic serum (NTS), targeting rat glomerular basement membrane to induce CGN. On day 4 and day 6, ON104 was given intraperitoneally (i.p.) and on day 8 urine, blood and kidney tissue were collected. ON104 substantially attenuated the severity of CGN demonstrated by reduced proteinuria, hematuria, as well as lower levels of kidney injury molecule (KIM)-1. ON104 treatment preserved the glomerular morphology and suppressed crescent formation, a hallmark of the disease. On the cellular level, oxMIF neutralization by ON104 strongly reduced the number of macrophages and neutrophils within the inflamed kidneys. In vitro, we identified human neutrophils, but not monocytes, as main producers of oxMIF among total peripheral cells. The present study demonstrates that oxMIF is a pertinent therapeutic target in a model of CGN which mechanistically resembles human immune mediated CGN. In this model, neutralization of oxMIF by ON104 leads to an improvement in both urinary abnormalities and histological pathological characteristics of the disease. ON104, thus has the potential to become a novel disease-modifying drug for the treatment of glomerulonephritis and other inflammatory kidney diseases.

Indexed as

GlomerulonephritisMacrophage Migration-Inhibitory FactorsAnimalsAntibodies, NeutralizingDisease Models, AnimalHumansKidneyMacrophagesMaleNeutrophilsOxidation-ReductionRabbitsRatsRats, Inbred WKYAntibodies, NeutralizingMacrophage Migration-Inhibitory Factors

Identifiers

PMID39374239
PMCPMC11458038

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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.