Evidence map›Paper›PMID 37055591›Full record

ArticleCell research2023

A lncRNA from an inflammatory bowel disease risk locus maintains intestinal host-commensal homeostasis.

Hongdi Ma, Taidou Hu, Wanyin Tao, Jiyu Tong, Zili Han, Dietmar Herndler-Brandstetter, Zheng Wei, Ruize Liu, Tingyue Zhou, Qiuyuan Liu and 8 more

Abstract read
In one paragraph

Article in Cell research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
–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

38 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  17. Non-coding RNA · 2025
    Review
  18. Article
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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.

Hongdi Ma *Department of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Taidou Hu *Department of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Wanyin TaoDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Jiyu TongDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
Zili HanDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Dietmar Herndler-BrandstetterDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
Zheng WeiDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID 0000-0002-1859-0374
Ruize LiuAnalytic and Translational Genetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Tingyue ZhouDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Qiuyuan LiuThe Key Laboratory of Digestive Diseases of Anhui Province, Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Xuemei XuDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Kaiguang ZhangDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Rongbin ZhouInstitute of Immunology, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.ORCID 0000-0002-3351-6420
Judy H ChoDepartment of Genetics, Yale School of Medicine, New Haven, CT, USA.
Hua-Bing LiShanghai Institute of Immunology, Department of Microbiology and Immunology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China. huabing.li@shsmu.edu.cn.ORCID 0000-0003-3573-6803
Hailiang HuangAnalytic and Translational Genetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. hhuang@broadinstitute.org.
Richard A FlavellDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA. richard.flavell@yale.edu.ORCID 0000-0003-4461-0778
Shu ZhuDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. zhushu@ustc.edu.cn.ORCID 0000-0002-8163-0869

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel diseases (IBD) are known to have complex, genetically influenced etiologies, involving dysfunctional interactions between the intestinal immune system and the microbiome. Here, we characterized how the RNA transcript from an IBD-associated long non-coding RNA locus ("CARINH-Colitis Associated IRF1 antisense Regulator of Intestinal Homeostasis") protects against IBD. We show that CARINH and its neighboring gene coding for the transcription factor IRF1 together form a feedforward loop in host myeloid cells. The loop activation is sustained by microbial factors, and functions to maintain the intestinal host-commensal homeostasis via the induction of the anti-inflammatory factor IL-18BP and anti-microbial factors called guanylate-binding proteins (GBPs). Extending these mechanistic insights back to humans, we demonstrate that the function of the CARINH/IRF1 loop is conserved between mice and humans. Genetically, the T allele of rs2188962, the most probable causal variant of IBD within the CARINH locus from the human genetics study, impairs the inducible expression of the CARINH/IRF1 loop and thus increases genetic predisposition to IBD. Our study thus illustrates how an IBD-associated lncRNA maintains intestinal homeostasis and protects the host against colitis.

Indexed as

ColitisInflammatory Bowel DiseasesRNA, Long NoncodingAnimalsHumansIntestinal MucosaIntestinesMiceRNA, Long Noncoding

Identifiers

PMID37055591
PMCPMC10156687

What OpenQuestion holds

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Registered trials

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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.