Evidence map›Paper›PMID 31129606›Full record

ArticleAnnals of the rheumatic diseases2019

Blockade of CCL24 with a monoclonal antibody ameliorates experimental dermal and pulmonary fibrosis.

Adi Mor, Michal Segal Salto, Avi Katav, Neta Barashi, Victoria Edelshtein, Mirko Manetti, Yair Levi, Jacob George, Marco Matucci-Cerinic

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

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  16. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
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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

9 authors at 5 institutions in 3 countries.

Adi MorR&D, ChemomAb Ltd, Tel Aviv, Israel.
Michal Segal SaltoR&D, ChemomAb Ltd, Tel Aviv, Israel michal@chemomab.com.ORCID 0000-0001-5061-8683
Avi KatavR&D, ChemomAb Ltd, Tel Aviv, Israel.
Neta BarashiR&D, ChemomAb Ltd, Tel Aviv, Israel.
Victoria EdelshteinR&D, ChemomAb Ltd, Tel Aviv, Israel.
Mirko ManettiDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy.
Yair LeviDepartment of Internal Medicine E, Meir Medical Center, Kfar-Saba, Israel.
Jacob GeorgeHeart Center, Kaplan Medical Center, Rehovot, Israel.
Marco Matucci-CerinicDepartment of Experimental and Clinical Medicine, University of Florence, Department of Geriatric Medicine, Division of Rheumatology and Scleroderma Unit, AOUC, Florence, Italy.
BSD Crown (Israel) · ILUniversity of Florence · ITChina National Building Materials Group (China) · CNKaplan Medical Center · ILMeir Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesWe aimed to assess the expression of the CCL24 chemokine in systemic sclerosis (SSc) and to evaluate the possible pathogenic implications of the CCL24/CCR3 axis using both in vitro and in vivo models. We further investigated the efficacy of an anti-CCL24 monoclonal antibody (mAb), CM-101, in inhibiting cell activation as well as dermal and pulmonary inflammation and fibrosis in experimental animal models.

methodsWe used ELISA and fluorescence immunohistochemistry to determine CCL24 levels in serum and CCL24/CCR3 expression in skin biopsies of SSc patients. Skin fibroblasts and endothelial cells treated with CCL24 or SSc serum with or without CM-101 were used to follow cell activation and differentiation. Prevention and treatment in vivo bleomycin (BLM)-induced models were used to evaluate experimental dermal and pulmonary fibrosis progression following treatment with the CM-101 mAb.

resultsCCL24 circulating levels were significantly elevated in SSc patients. CCL24/CCR3 expression was strongly increased in SSc skin. Blockade of CCL24 with CM-101 significantly reduced the activation of dermal fibroblasts and their transition to myofibroblasts induced by SSc serum. CM-101 was also able to significantly inhibit endothelial cell activation induced by CCL24. In BLM-induced experimental animal models, CM-101 profoundly inhibited both dermal and pulmonary fibrosis and inflammation.

conclusionsCCL24 plays an important role in pathological processes of skin and lung inflammation and fibrosis. Inhibition of CCL24 by CM-101 mAb can be potentially beneficial for therapeutic use in SSc patients.

Indexed as

AnimalsAntibodies, MonoclonalCell DifferentiationCells, CulturedChemokine CCL24Disease Models, AnimalFemaleFibroblastsFibrosisHumansMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutPolysaccharides, BacterialAntibodies, MonoclonalChemokine CCL24Polysaccharides, Bacterialstreptococcal polysaccharide type III group Bchemokinesinflammationpulmonary fibrosissystemic sclerosis

Identifiers

PMID31129606
PMCPMC6788878
OpenAlexW2945882197

What OpenQuestion holds

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LicenceCC BY-NC
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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.