Evidence map›Paper›PMID 32079724›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

CUX1 and IκBζ (NFKBIZ) mediate the synergistic inflammatory response to TNF and IL-17A in stromal fibroblasts.

Kamil Slowikowski, Hung N Nguyen, Erika H Noss, Daimon P Simmons, Fumitaka Mizoguchi, Gerald F M Watts, Michael F Gurish, Michael B Brenner, Soumya Raychaudhuri

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.5field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
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  7. Evaluation of ATP12A and NFKBIZ as potential markers of inflammatory status in cystic fibrosis airway epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  16. IĸBζ as a Central Modulator of Inflammatory Arthritis Pathogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Article
  17. Review
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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 3 institutions in 3 countries.

Kamil SlowikowskiDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-2843-6370
Hung N NguyenDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Erika H NossDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Daimon P SimmonsDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Fumitaka MizoguchiDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 113-8519 Tokyo, Japan.ORCID 0000-0002-3956-7122
Gerald F M WattsDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Michael F GurishDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Michael B BrennerDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; mbrenner@research.bwh.harvard.edu soumya@broadinstitute.org.
Soumya RaychaudhuriDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; mbrenner@research.bwh.harvard.edu soumya@broadinstitute.org.
Brigham and Women's Hospital · USBroad Institute · USTokyo Medical and Dental University · JP

Funding

Metabolomics Core U19AI111224 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI MURRAY, MEGAN, MURRAY, MEGAN B · 2015 to 2021
$20.4M
Training Program in Bioinformatics and Integrative GenomicsT32HG002295 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Peter J Park · 2001 to 2026
$15.8M
VASCULAR, PULMONARY AND RENAL INJURYT32HL007627 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A, MITCHELL, RICHARD N · 1985 to 2019
$12.7M
Genetic predictors of response to anti-TNF therapy in rheumatoid arthritisU01GM092691 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B., RAYCHAUDHURI, SOUMYA · 2010 to 2014
$7.5M
RA-SLE Molecular Deconstruction Leadership CenterUH2AR067677 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B., RAYCHAUDHURI, SOUMYA · 2014 to 2020
$4.3M
Expanded fibroblast subset drives pathology in rheumatoid arthritisR01AR063709 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B., RAYCHAUDHURI, SOUMYA · 2015 to 2025
$3.3M
Functionally specialized components of disease heritability in ENCODE dataU01HG009379 · NHGRI · HARVARD SCHOOL OF PUBLIC HEALTH · PI PRICE, ALKES L, RAYCHAUDHURI, SOUMYA · 2017 to 2021
$2.5M
Deciphering Pathways Driving Inflammatory Fibroblast Effector Functions in RAR01AR073833 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B. · 2019 to 2023
$1.9M
Transcriptomics in synoviocytes defines pathogenesis of rheumatoid arthritisF31AR070582 · NIAMS · HARVARD MEDICAL SCHOOL · PI SLOWIKOWSKI, KAMIL · 2016 to 2017
$63k
Medical Research Council MR/R013926/1NHGRI NIH HHS T32 HG002295NHGRI NIH HHS U01 HG009379NHLBI NIH HHS T32 HL007627NIAID NIH HHS U19 AI111224NIAMS NIH HHS F31 AR070582NIAMS NIH HHS R01 AR063709NIAMS NIH HHS R01 AR073833NIAMS NIH HHS UH2 AR067677NIGMS NIH HHS U01 GM092691
6 · The paper itself

Abstract

The role of stromal fibroblasts in chronic inflammation is unfolding. In rheumatoid arthritis, leukocyte-derived cytokines TNF and IL-17A work together, activating fibroblasts to become a dominant source of the hallmark cytokine IL-6. However, IL-17A alone has minimal effect on fibroblasts. To identify key mediators of the synergistic response to TNF and IL-17A in human synovial fibroblasts, we performed time series, dose-response, and gene-silencing transcriptomics experiments. Here we show that in combination with TNF, IL-17A selectively induces a specific set of genes mediated by factors including cut-like homeobox 1 (CUX1) and IκBζ (NFKBIZ). In the promoters of

Indexed as

Adaptor Proteins, Signal TransducingArthritis, RheumatoidCells, CulturedChemokine CXCL1Chemokine CXCL2Chemokines, CXCChemotactic FactorsFibroblastsHomeodomain ProteinsHumansInflammationInterleukin-17Interleukin-6Matrix Metalloproteinase 3MonocytesRepressor ProteinsAdaptor Proteins, Signal TransducingChemokine CXCL1Chemokine CXCL2Chemokines, CXCChemotactic FactorsCUX1 protein, humanCXCL1 protein, humanCXCL2 protein, humanCXCL3 protein, humanHomeodomain ProteinsIL6 protein, humanInterleukin-17Interleukin-6Matrix Metalloproteinase 3NFKBIZ protein, humanRELA protein, humanRepressor ProteinsRNA, Small InterferingTranscription Factor RelATranscription FactorsTumor Necrosis Factor-alphainflammationregulationRNA-seqtime seriestranscription

Identifiers

PMID32079724
PMCPMC7071902
OpenAlexW3007823876

What OpenQuestion holds

Textmetadata
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.