Evidence map›Paper›PMID 39396665›Full record

ArticleMucosal immunology2025

TRIM29 controls enteric RNA virus-induced intestinal inflammation by targeting NLRP6 and NLRP9b signaling pathways.

Junying Wang, Ling Wang, Wenting Lu, Naser Farhataziz, Anastasia Gonzalez, Junji Xing, Zhiqiang Zhang

Abstract read
In one paragraph

Article in Mucosal immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

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

  1. Pooled it
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  11. Role of Nod-like Receptors inMicroorganisms · 2026
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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

7 authors.

Junying WangImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA.
Ling WangImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA; Department of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun, 130021, China.
Wenting LuImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA.
Naser FarhatazizImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA.
Anastasia GonzalezImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA.
Junji XingImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA; Department of Cardiovascular Sciences, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA; Department of Surgery, Weill Cornell Medicine, Cornell University, New York, NY 10065, USA. Electronic address: jxing@houstonmethodist.org.
Zhiqiang ZhangImmunobiology and Transplant Science Center, Department of Surgery, Houston Methodist Academic Institute, Houston Methodist, Houston, TX 77030, USA; Department of Surgery, Weill Cornell Medicine, Cornell University, New York, NY 10065, USA. Electronic address: zzhang@houstonmethodist.org.

Funding

Studies of a new checkpoint regulator in the control of intestinal inflammationR01AI155488 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ZHANG, ZHIQIANG · 2021 to 2025
$2.0M
NIAID NIH HHS R01 AI155488
6 · The paper itself

Abstract

Infections by enteric virus and intestinal inflammation are recognized as a leading cause of deadly gastroenteritis, and NLRP6 and NLRP9b signaling control these infection and inflammation. However, the regulatory mechanisms of the NLRP6 and NLRP9b signaling in enteric viral infection remain unexplored. In this study, we found that the E3 ligase TRIM29 suppressed type III interferon (IFN-λ) and interleukin-18 (IL-18) production by intestinal epithelial cells (IECs) when exposed to polyinosinic:polycytidylic acid (poly I:C) and enteric RNA viruses. Knockout of TRIM29 in IECs was efficient to restrict intestinal inflammation triggered by the enteric RNA viruses, rotavirus in suckling mice, and the encephalomyocarditis virus (EMCV) in adults. This attenuation in inflammation was attributed to the increased production of IFN-λ and IL-18 in the IECs and more recruitment of intraepithelial protective Ly6A

Indexed as

Adaptor Proteins, Signal TransducingDNA-Binding ProteinsEncephalomyocarditis virusInflammationIntestinal MucosaRNA VirusesRNA Virus InfectionsRotavirusTranscription FactorsAnimalsHumansInterferon LambdaInterferonsInterleukin-18InterleukinsMiceAdaptor Proteins, Signal TransducingDNA-Binding ProteinsInterferon Lambdainterferon-lambda protein, mouseInterferonsInterleukin-18InterleukinsNod-like receptor pyrin domain-containing protein 6, mouseReceptors, Cell SurfaceTranscription Factors

Identifiers

PMID39396665
PMCPMC12210021

What OpenQuestion holds

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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.