Evidence map›Paper›PMID 37813481›Full record

ArticleAnnals of the rheumatic diseases2024

Card9/neutrophil signalling axis promotes IL-17A-mediated ankylosing spondylitis.

Holly L Rosenzweig, Emily E Vance, Kofi Asare-Konadu, Kylie V Koney, Ellen J Lee, Atul A Deodhar, Rouhin Sen, Liron Caplan, Ruth J Napier

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.2field-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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  17. CARD9 in the pathogenesis of axial spondyloarthritis.Best practice & research. Clinical rheumatology · 2024
    Review
  18. CRISPR-Cas9 applications in T cells and adoptive T cell therapies.Cellular & molecular biology letters · 2024
    Review
  19. Review
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 1 country.

Holly L RosenzweigMolecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA.
Emily E VanceMolecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA.ORCID http://orcid.org/0000-0001-8289-2775
Kofi Asare-KonaduMolecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA.
Kylie V KoneyPortland VA Medical Center, Portland, Oregon, USA.
Ellen J LeeMolecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA.
Atul A DeodharDiv Arthritis/Rheumatic Diseases, Oregon Health & Science University, Portland, Oregon, USA.ORCID http://orcid.org/0000-0002-2130-1246
Rouhin SenUniversity of Colorado, Denver, Colorado, USA.
Liron CaplanVA Eastern Colorado Health Care System, Aurora, Colorado, USA.
Ruth J NapierMolecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA napier@ohsu.edu.ORCID http://orcid.org/0000-0002-2785-8248
Oregon Health & Science University · USVA Eastern Colorado Health Care System · USPortland VA Medical Center · US

Funding

Research Training in Rheumatology INCLUDE Down Syndrome SupplementT32AR007534 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI Kristine A. Kuhn · 1986 to 2026
$6.1M
Innate Immunity and its integration in Autoimmune Disease of the EyeR01EY025250 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ROSENZWEIG, HOLLY LALLMAN · 2015 to 2023
$2.7M
Interaction of environment and genetics in the predisposition to inflammatory artI01BX002180 · VA · PORTLAND VA MEDICAL CENTER · PI ROSENZWEIG, HOLLY LALLMAN · 2014 to 2021
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CARD9 in Ankylosing SpondylitisI01BX006436 · VA · PORTLAND VA MEDICAL CENTER · PI NAPIER, RUTH · 2024 to 2025
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Reprogramming T Cells in Rheumatoid ArthritisIK2BX004523 · VA · PORTLAND VA MEDICAL CENTER · PI NAPIER, RUTH · 2019 to 2023
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BLRD VA I01 BX002180BLRD VA I01 BX006436BLRD VA IK2 BX004523NEI NIH HHS R01 EY025250NIAMS NIH HHS T32 AR007534
6 · The paper itself

Abstract

objectivePolymorphisms in the antifungal signalling molecule

methodsExperiments in SKG, Card9

resultsCard9 functioned downstream of Dectin-1 and was essential for induction of Th17 cells, arthritis and spondylitis in SKG mice. Card9 expression within T cells was dispensable for arthritis onset in SKG mice. Rather, Card9 expression controlled neutrophil function; and neutrophils in turn, were responsible for triggering Th17 expansion and disease in SKG mice. Mechanistically, cocultures of zymosan prestimulated neutrophils and SKG T cells revealed a direct cellular function for Card9 within neutrophils in the potentiation of IL-17 production by CD4

conclusionsThese data reveal a novel neutrophil-intrinsic role for Card9 in arthritogenic Th17 responses and AS pathogenesis. These data provide valuable utility in our future understanding of CARD9-specific mechanisms in spondyloarthritis .

Indexed as

SpondylarthritisSpondylitis, AnkylosingAnimalsCARD Signaling Adaptor ProteinsCoculture TechniquesHumansInterleukin-17MiceNeutrophilsTh17 CellsCard9 protein, mouseCARD Signaling Adaptor ProteinsInterleukin-17ArthritisArthritis, ExperimentalAutoimmunitySpondylitis, AnkylosingT-Lymphocyte subsets

Identifiers

PMID37813481
PMCPMC10850635
OpenAlexW4387451191

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.