Evidence map›Paper›PMID 32381123›Full record

ArticleArthritis research & therapy2020

Circulating TNF-like protein 1A (TL1A) is elevated early in rheumatoid arthritis and depends on TNF.

Yun-Jeong Song, In Ah Choi, Françoise Meylan, M Kristen Demoruelle, Taylor Farley, Arianne C Richard, Eric Hawley, John Botson, Yoo Jin Hong, Eun Young Lee and 19 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 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

29 authors at 10 institutions in 2 countries.

Yun-Jeong SongImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
In Ah ChoiDivision of Rheumatology, Department of Internal Medicine, MMBS, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea.
Françoise MeylanImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
M Kristen DemoruelleDivision of Rheumatology, University of Colorado School of Medicine, Aurora, CO, 80207, USA.
Taylor FarleyImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
Arianne C RichardImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
Eric HawleyImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
John BotsonImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA.
Yoo Jin HongDivision of Rheumatology, Department of Internal Medicine, MMBS, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea.
Eun Young LeeDivision of Rheumatology, Department of Internal Medicine, MMBS, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea.
Sabina R MianDivision of Rheumatology, Department of Medicine, Los Angeles County University of Southern California Medical Center and University of Southern California Keck School of Medicine, Los Angeles, CA, USA.
Bartlett C HamiltonRheumatology Division, Department of Medicine, University of Nebraska Medical Center and VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Geoffrey M ThieleRheumatology Division, Department of Medicine, University of Nebraska Medical Center and VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Ted R MikulsRheumatology Division, Department of Medicine, University of Nebraska Medical Center and VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Naveen GaraLiver Diseases Branch, NIDDK, NIH, Bethesda, MD, USA.
Chris D WardHuman Genome Sciences, Rockville, MD, USA.
Sarah LamberthImmunology Biomarkers group, Pharmaceutical Companies of J&J, LLC, Spring House, PA, USA.
Kevin D DeaneDivision of Rheumatology, University of Colorado School of Medicine, Aurora, CO, 80207, USA.
Theo HellerLiver Diseases Branch, NIDDK, NIH, Bethesda, MD, USA.
Michael M WardClinical Trials and Outcomes Branch, NIAMS, NIH, Bethesda, MD, USA.
David M LeeBrigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Thi-Sau MigoneHuman Genome Sciences, Rockville, MD, USA.
William StohlDivision of Rheumatology, Department of Medicine, Los Angeles County University of Southern California Medical Center and University of Southern California Keck School of Medicine, Los Angeles, CA, USA.
James R O'DellRheumatology Division, Department of Medicine, University of Nebraska Medical Center and VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Jill M NorrisColorado School of Public Health, Aurora, CO, USA.
V Michael HolersDivision of Rheumatology, University of Colorado School of Medicine, Aurora, CO, 80207, USA.
Peter GregersenCenter for Genomics & Human Genetics, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, Manhasset, NY, USA.
Yeong-Wook SongDivision of Rheumatology, Department of Internal Medicine, MMBS, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea.
Richard M SiegelImmunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD, USA. richardmsiegel@gmail.com.ORCID 0000-0001-5953-9893
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USSeoul National University · KRVA Nebraska Western Iowa Health Care System · USNational Institutes of Health · USUniversity of Colorado Denver · USHuman Genome Sciences (United States) · USUniversity of Southern California · USBrigham and Women's Hospital · USColorado School of Public Health · USFeinstein Institute for Medical Research · US

Funding

Investigation of management and disease manifestations of viral hepatitisZIADK054514 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HELLER, THEO · 2009 to 2025
$12.9M
Prevention Center U01: Early Targets for Antigen-Specific Tolerance Induction in Preclinical Rheumatoid ArthritisU01AI101981 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2012 to 2021
$6.2M
The Lung as an Originating Site of Autoimmunity in Rheumatoid ArthritisK23AR066712 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI DEMORUELLE, M. KRISTEN · 2014 to 2018
$776k
National Institute of Allergy and Infectious Diseases AI101981NIAID NIH HHS U01 AI101981NIAMS NIH HHS AR066712NIAMS NIH HHS IntramuralNIAMS NIH HHS K23 AR066712
6 · The paper itself

Abstract

backgroundThe tumor necrosis factor (TNF) superfamily cytokine TNF-like protein 1A (TL1A) and its receptor DR3 are essential for diverse animal models of autoimmune disease and may be pathogenic in rheumatoid arthritis (RA). However, the relationship of TL1A to disease duration, activity, and response to anti-TNF and other therapies in RA is not clear.

methodsWe measured soluble TL1A in synovial fluid (SF), serum, or plasma from RA first-degree relatives (FDRs) and in early RA and established disease. We measured the effects of anti-TNF and methotrexate (MTX) therapy on circulating TL1A from multiple independent RA treatment trials. We also determined the ability of a blocking anti-TL1A antibody to inhibit clinical disease and articular bone destruction in the murine collagen-induced arthritis (CIA) model of human RA.

resultsSoluble TL1A was specifically elevated in the blood and SF of patients with RA compared to patients with other diseases and was elevated early in disease and in at-risk anti-cyclic citrullinated peptide (CCP) (+) first-degree relatives (FDRs). Therapeutic TNF inhibition reduced serum TL1A in both responders and non-responders, whereas TL1A declined following MTX treatment only in responders. In murine CIA, TL1A blockade was clinically efficacious and reduced bone erosions.

conclusionsTL1A is specifically elevated in RA from early in the disease course and in at-risk FDRs. The decline in TL1A after TNF blockade suggests that TL1A levels may be a useful biomarker for TNF activity in RA. These results support the further investigation of the relationship between TL1A and TNF and TL1A blockade as a potential therapeutic strategy in RA.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAnimalsHumansMethotrexateMiceSynovial FluidTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsTumor Necrosis Factor Ligand Superfamily Member 15MethotrexateTNFSF15 protein, humanTnfsf15 protein, mouseTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsTumor Necrosis Factor Ligand Superfamily Member 15Collagen-induced arthritisCytokinesRheumatoid arthritisTNFSF15Tumor necrosis factor-like cytokine 1A

Identifiers

PMID32381123
PMCPMC7204024
OpenAlexW3022302110

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.