Evidence map›Paper›PMID 42238449›Full record

ArticlemedRxiv : the preprint server for health sciences2026

Long Noncoding RNA Associations Define an Interferon-Myeloid Immune Axis in Kawasaki Disease.

Fang Liu, Xing Xue, Zhi Han, Bo Jin, Weiwei Li, Naoto Ozawa, Takumi Ichikawa, Ellen Ling, Xinyang Zhao, Henry Chubb and 6 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Fang LiuHeart Center, Children's Hospital of Fudan University, Shanghai, China.
Xing XueHeart Center, Children's Hospital of Fudan University, Shanghai, China.
Zhi HanSchool of Medicine, Stanford University, Stanford, CA, USA.
Bo JinOncoOmicsDx Clinical Laboratory, Rockville, MD, USA.
Weiwei LiOncoOmicsDx Clinical Laboratory, Rockville, MD, USA.
Naoto OzawaSchool of Medicine, Stanford University, Stanford, CA, USA.
Takumi IchikawaSchool of Medicine, Stanford University, Stanford, CA, USA.
Ellen LingFlorida State University, Tallahassee, FL 32306, USA.
Xinyang ZhaoUniversity of Kansas Medical Center, Kansas City, KS 66160, USA.
Henry ChubbSchool of Medicine, Stanford University, Stanford, CA, USA.
Scott R CeresnakSchool of Medicine, Stanford University, Stanford, CA, USA.
Gary L DarmstadtSchool of Medicine, Stanford University, Stanford, CA, USA.
Doff B McElhinneySchool of Medicine, Stanford University, Stanford, CA, USA.
Harvey J CohenSchool of Medicine, Stanford University, Stanford, CA, USA.
Seda TierneySchool of Medicine, Stanford University, Stanford, CA, USA.ORCID 0000-0002-4654-3794
Xuefeng B LingSchool of Medicine, Stanford University, Stanford, CA, USA.

Funding

An automated system to differentiate Kawasaki disease from febrile illness with real life clinical datasets in New York CityR41TR004351 · NCATS · HBI SOLUTIONS INC. · PI SCHILLING, JAMES W · 2022 to 2022
$346k
NCATS NIH HHS R41 TR004351
6 · The paper itself

Abstract

Kawasaki disease (KD) is an acute pediatric vasculitis characterized by dysregulated host immune responses and risk of coronary artery injury. Although a two-transcript IFI27-MCEMP1 axis has been clinically validated to distinguish KD from other febrile illnesses, the long noncoding RNA (lncRNA) context of this interferon-myeloid imbalance remains incompletely understood. We evaluated whether peripheral blood mononuclear cell (PBMC)-derived lncRNAs are altered in KD and associated with the interferon and myeloid components of the IFI27-MCEMP1 transcriptomic axis. Children younger than 8 years with suspected KD were prospectively enrolled at the Children's Hospital of Fudan University from 2024 to 2025. The newly enrolled cohort included 55 children with KD and 48 febrile controls. For integrated immune-transcript association analyses, these data were combined with two previously characterized same-site cohorts, yielding 188 children with KD and 175 febrile controls. Expression of IFI27, MCEMP1, CHROMR, MALAT1, and NEAT1 was measured by reverse transcription quantitative PCR and normalized to GAPDH using ΔCt values. In the newly enrolled cohort, the IFI27-MCEMP1 axis reproduced discrimination between KD and febrile controls, with an area under the receiver operating characteristic curve of 0.88; performance was similar in the integrated cohort, with an area under the curve of 0.89. In PBMC lncRNA analyses, CHROMR and MALAT1 ΔCt values were significantly higher in KD than in febrile controls, indicating lower relative expression, whereas NEAT1 did not show a significant KD-specific differential-expression signal. CHROMR showed the strongest association with the IFI27 interferon-associated component, while MALAT1 showed weaker but directionally informative associations with both IFI27 and MCEMP1, including an inverse association with MCEMP1. These findings support an lncRNA-associated interferon-myeloid immune architecture in KD, marked by coordinated attenuation of IFI27, CHROMR, and MALAT1 together with increased MCEMP1. This PBMC RNA pattern provides a biologically interpretable framework for KD immune dysregulation and generates testable hypotheses regarding RNA-regulatory programs in KD vasculitis.

Identifiers

PMID42238449
PMCPMC13228753

What OpenQuestion holds

Textmetadata
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.