Evidence map›Paper›PMID 30092201›Full record

ArticleCell host & microbe2018

LIGHT-HVEM Signaling in Innate Lymphoid Cell Subsets Protects Against Enteric Bacterial Infection.

Goo-Young Seo, Jr-Wen Shui, Daisuke Takahashi, Christina Song, Qingyang Wang, Kenneth Kim, Zbigniew Mikulski, Shilpi Chandra, Daniel A Giles, Sonja Zahner and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cell host & microbe, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  7. Group 1 innate lymphoid cells protect liver transplants from ischemia-reperfusion injury via an interferon gamma-mediated pathway.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Article
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  19. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  20. Article
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

14 authors at 4 institutions in 2 countries.

Goo-Young SeoDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA; Department of Molecular Bioscience, School of Biomedical Science and Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 24341, Republic of Korea.
Jr-Wen ShuiDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Daisuke TakahashiDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Christina SongDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Qingyang WangDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Kenneth KimDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Zbigniew MikulskiMicroscopy and Histology Core, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Shilpi ChandraDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Daniel A GilesDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Sonja ZahnerDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Pyeung-Hyeun KimDepartment of Molecular Bioscience, School of Biomedical Science and Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 24341, Republic of Korea.
Hilde CheroutreDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Mitchell KronenbergDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA; Division of Biology, University of California San Diego, La Jolla, CA 92037, USA. Electronic address: mitch@lji.org.
La Jolla Institute for Immunology · USWashington University in St. Louis · USKangwon National University · KRUniversity of California, San Diego · US

Funding

Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
The role of LIGHT in Colitis PathogenesisR01AI061516 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2004 to 2015
$4.5M
Control of the Functional Fate of CD4 T Cells by LncRNA-SwitchU01AI125957 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CHEROUTRE, HILDE MC · 2016 to 2020
$2.7M
HVEM: A TNF family receptor that influences mucosal immunity and the microbiomeU01AI125955 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2016 to 2020
$2.7M
FACSAria II Cell SorterS10RR027366 · NCRR · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 2011 to 2011
$514k
NCRR NIH HHS S10 RR027366NIAID NIH HHS R01 AI061516NIAID NIH HHS U01 AI125955NIAID NIH HHS U01 AI125957NIDDK NIH HHS P01 DK046763
6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) are important regulators of early infection at mucosal barriers. ILCs are divided into three groups based on expression profiles, and are activated by cytokines and neuropeptides. Yet, it remains unknown if ILCs integrate other signals in providing protection. We show that signaling through herpes virus entry mediator (HVEM), a member of the tumor necrosis factor (TNF) receptor superfamily, in ILC3 is important for host defense against oral infection with the bacterial pathogen Yersinia enterocolitica. HVEM stimulates protective interferon-γ (IFN-γ) secretion from ILCs, and mice with HVEM-deficient ILC3 exhibit reduced IFN-γ production, higher bacterial burdens and increased mortality. In addition, IFN-γ production is critical as adoptive transfer of wild-type but not IFN-γ-deficient ILC3 can restore protection to mice lacking ILCs. We identify the TNF superfamily member, LIGHT, as the ligand inducing HVEM signals in ILCs. Thus HVEM signaling mediated by LIGHT plays a critical role in regulating ILC3-derived IFN-γ production for protection following infection. VIDEO ABSTRACT.

Indexed as

Signal TransductionAdoptive TransferAdultAnimalsCytokinesDisease Models, AnimalEnterobacteriaceae InfectionsHomeodomain ProteinsHost-Pathogen InteractionsHumansInterferon-gammaLymphocytesMaleMiceMice, Inbred C57BLMice, KnockoutCCR6 protein, mouseCytokinesHomeodomain ProteinsInterferon-gammaNeuropeptidesRAG-1 proteinReceptors, CCR6Receptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Member 14Tnfsf14 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 14CCR6HVEMIFN-γileuminfectioninnate lymphoid cellsLIGHTYersinia enterocolitica

Identifiers

PMID30092201
PMCPMC6132068
OpenAlexW2885660114

What OpenQuestion holds

Textmetadata
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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.