Evidence map›Paper›PMID 31174578›Full record

ArticleArthritis research & therapy2019

Depletion of activated macrophages with a folate receptor-beta-specific antibody improves symptoms in mouse models of rheumatoid arthritis.

Yingwen Hu, Bingbing Wang, Jiayin Shen, Stewart A Low, Karson S Putt, Hans W M Niessen, Eric L Matteson, Linda Murphy, Clemens Ruppert, Gerrit Jansen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.8field-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

25 citing papers in PubMed, 44 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

15 authors at 9 institutions in 3 countries.

Yingwen HuDepartment of Chemistry, Purdue University, 560 Oval Drive, West Lafayette, IN, 47907, USA.
Bingbing WangDepartment of Chemistry, Purdue University, 560 Oval Drive, West Lafayette, IN, 47907, USA.
Jiayin ShenDepartment of Chemistry, Purdue University, 560 Oval Drive, West Lafayette, IN, 47907, USA.
Stewart A LowDepartment of Chemistry, Purdue University, 560 Oval Drive, West Lafayette, IN, 47907, USA.
Karson S PuttInstitute for Drug Discovery, Purdue University, West Lafayette, IN, 47907, USA.
Hans W M NiessenDepartment of Pathology and Cardiac Surgery, ACS, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands.
Eric L MattesonDivision of Rheumatology, and Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Linda MurphyDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Clemens RuppertJustus-Liebig University Giessen, Department of Internal Medicine, Biomedizinisches Forschungszentrum Seltersberg, Giessen, Germany.
Gerrit JansenDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, VU University Medical Center, Amsterdam, The Netherlands.
Stephen J OliverDepartment of Medicine, New York University School of Medicine, New York, NY, USA.
Yang FengProtein Interactions Section, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer, National Cancer Institute-Frederick, National Institutes of Health, Frederick, MD, 21702, USA.
Dimiter S DimitrovCenter for Antibody Therapeutics, University of Pittsburgh, Pittsburgh, PA, 15216, USA.
Cheryl Nickerson-NutterHuLow Medical, Northbrook, IL, USA.
Philip S LowDepartment of Chemistry, Purdue University, 560 Oval Drive, West Lafayette, IN, 47907, USA. plow@purdue.edu.
Purdue University West Lafayette · USAmsterdam UMC Location VUmc · NLAmsterdam University Medical Centers · NLFrederick National Laboratory for Cancer Research · USMayo Clinic · USMayo Clinic in Florida · USNew York University · USUniversity of Giessen · DEUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMost therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages.

methodsFirst, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis.

resultsHuman tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions.

conclusionsThese data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages.

Indexed as

Immunity, CellularMacrophage ActivationAnimalsAntibodies, MonoclonalArthritis, RheumatoidCells, CulturedCytokinesDisease Models, AnimalFolate Receptor 2HumansMacrophagesMiceAntibodies, MonoclonalCytokinesFolate Receptor 2Activated macrophagesAutoimmune diseaseFolate receptor betaInflammatory diseaseRheumatoid arthritis

Identifiers

PMID31174578
PMCPMC6555977
OpenAlexW2952442195

What OpenQuestion holds

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LicenceCC BY
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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.