Evidence map›Paper›PMID 36804906›Full record

ArticleArthritis research & therapy2023

Identification of anti-citrullinated osteopontin antibodies and increased inflammatory response by enhancement of osteopontin binding to fibroblast-like synoviocytes in rheumatoid arthritis.

Akio Umemoto, Takeshi Kuwada, Koichi Murata, Masahiro Shiokawa, Sakiko Ota, Yoshiki Murotani, Akihiro Itamoto, Kohei Nishitani, Hiroyuki Yoshitomi, Takayuki Fujii and 8 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

5 citing papers in PubMed, 8 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 1 institution in 1 country.

Akio Umemoto *Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Takeshi Kuwada *Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan.
Koichi Murata *Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan. kchm@kuhp.kyoto-u.ac.jp.ORCID 0000-0002-7896-3937
Masahiro Shiokawa *Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan. machan@kuhp.kyoto-u.ac.jp.ORCID 0000-0001-6436-3888
Sakiko OtaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan.
Yoshiki MurotaniDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Akihiro ItamotoDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Kohei NishitaniDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Hiroyuki YoshitomiDepartment of Immunology, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8501, Japan.
Takayuki FujiiDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Akira OnishiDepartment of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine, 54 Kawahara-Cho, Shogoin, Sakyo, Kyoto, 606-8507, Japan.
Hideo OnizawaDepartment of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine, 54 Kawahara-Cho, Shogoin, Sakyo, Kyoto, 606-8507, Japan.
Kosaku MurakamiCenter for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Masao TanakaDepartment of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine, 54 Kawahara-Cho, Shogoin, Sakyo, Kyoto, 606-8507, Japan.
Hiromu ItoDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Hiroshi SenoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan.
Akio MorinobuDepartment of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Shuichi MatsudaDepartment of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8507, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnti-citrullinated protein/peptide antibodies (ACPAs) are present in patients at onset and have important pathogenic roles during the course of rheumatoid arthritis (RA). The characteristics of several molecules recognized by ACPA have been studied in RA, but the positivity rate of autoantibodies against each antigen is not high, and the pathogenic mechanism of each antibody is not fully understood. We investigated the role of anti-citrullinated osteopontin (anti-cit-OPN) antibodies in RA pathogenesis.

methodsEnzyme-linked immunosorbent assays on RA patients' sera were used to detect autoantibodies against OPN. Fibroblast-like synoviocytes (FLS) isolated from RA patients were used to test the binding activity and inflammatory response of OPN mediated by anti-cit-OPN antibodies, and their effect was tested using an inflammatory arthritis mouse model immunized with cit-OPN. Anti-cit-OPN antibody positivity and clinical characteristics were investigated in the patients as well.

resultsUsing sera from 224 RA patients, anti-cit-OPN antibodies were positive in approximately 44% of RA patients, while approximately 78% of patients were positive for the cyclic citrullinated peptide (CCP2) assay. IgG from patients with anti-cit-OPN antibody increased the binding activity of OPN to FLSs, which further increased matrix metalloproteinase and interleukin-6 production in TNF-stimulated FLSs. Mice immunized with cit-OPN antibodies experienced severe arthritis. Anti-cit-OPN antibodies in RA patients decreased the drug survival rate of tumor necrosis factor (TNF) inhibitors, while it did not decrease that of CTLA4-Ig.

conclusionsAnti-cit-OPN antibodies were detected in patients with RA. IgG from patients with anti-cit-OPN antibodies aggravated RA, and anti-cit-OPN antibody was a marker of reduced the survival rate of TNF inhibitors in RA patients.

Indexed as

Arthritis, RheumatoidSynoviocytesAnimalsAnti-Citrullinated Protein AntibodiesAutoantibodiesFibroblastsImmunoglobulin GMiceOsteopontinAnti-Citrullinated Protein AntibodiesAutoantibodiesImmunoglobulin GOsteopontinAnti-citrullinated protein antibodyCitrullinationIntegrinOsteopontinRheumatoid arthritis

Identifiers

PMID36804906
PMCPMC9936655
OpenAlexW4321242121

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LicenceCC BY
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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.