Evidence map›Paper›PMID 39464882›Full record

ArticleFrontiers in immunology2024

Toll-like receptor 7 protects against intestinal inflammation and restricts the development of colonic tissue-resident memory CD8

Hussein Hamade, Masato Tsuda, Naoki Oshima, Dalton T Stamps, Michelle H Wong, Jasmine T Stamps, Lisa S Thomas, Brenda C Salumbides, Caroline Jin, Jordan S Nunnelee and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 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

13 authors.

Hussein HamadeF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Masato TsudaF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Naoki OshimaF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Dalton T StampsF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Michelle H WongF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Jasmine T StampsF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Lisa S ThomasF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Brenda C SalumbidesF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Caroline JinF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Jordan S NunneleeF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Deepti DhallDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Stephan R TarganF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Kathrin S MichelsenF. Widjaja Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The maintenance of intestinal homeostasis depends on a complex interaction between the immune system, intestinal epithelial barrier, and microbiota. Alteration in one of these components could lead to the development of inflammatory bowel diseases (IBD). Variants within the autophagy gene Results and discussion: However, the role of the enteric virome in IBD is still poorly understood. Here, we investigate the role of TLR7 and ATG16L1 in intestinal homeostasis and inflammation. At steady state, Conclusion: In conclusion, the convergence of ATG16L1 and TLR7 signaling pathways plays an important role in the immune response to intestinal viruses. Our data suggest that activation of the TLR7 signaling pathway could be an attractive therapeutic target for CD patients with

Indexed as

Autophagy-Related ProteinsCD8-Positive T-LymphocytesImmunologic MemoryMice, KnockoutToll-Like Receptor 7AnimalsCaliciviridae InfectionsColitisColonDisease Models, AnimalIntestinal MucosaMembrane GlycoproteinsMiceMice, Inbred C57BLNorovirusAtg16l1 protein, mouseAutophagy-Related ProteinsMembrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7ATG16L1autophagyCD8+ Trminflammatory bowel diseasesplasmacytoid dendritic cellsTLR7

Identifiers

PMID39464882
PMCPMC11502343

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.