Evidence map›Paper›PMID 29623414›Full record

ReviewSeminars in immunopathology2018

ILC2s in infectious diseases and organ-specific fibrosis.

Markus Kindermann, Lisa Knipfer, Imke Atreya, Stefan Wirtz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Discriminative Role of Interleukin-6, Neuropilin-1, and Amphiregulin for Cirrhosis in Patients with Chronic Hepatitis B Infection.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
    Article
  2. Review
  3. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Frontiers in cellular and infection microbiology · 2022
    Review
  8. Review
  9. Review
  10. CCR8 SignalingFrontiers in immunology · 2020
    Article
  11. Innate Lymphoid Cells in Crohn's Disease.Frontiers in immunology · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Markus KindermannDepartment of Medicine 1, Friedrich-Alexander-University Erlangen-Nuremberg, 91052, Erlangen, Germany.
Lisa KnipferDepartment of Medicine 1, Friedrich-Alexander-University Erlangen-Nuremberg, 91052, Erlangen, Germany.
Imke AtreyaDepartment of Medicine 1, Friedrich-Alexander-University Erlangen-Nuremberg, 91052, Erlangen, Germany.
Stefan WirtzDepartment of Medicine 1, Friedrich-Alexander-University Erlangen-Nuremberg, 91052, Erlangen, Germany. stefan.wirtz@uk-erlangen.de.ORCID 0000-0001-6936-7431
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 immune responses evolved to provide host protection against parasitic infections and to support the repair of infection-induced tissue injury. However, persistent chronic organ damage can result in dysregulated production of critical type 2 cytokines supporting tissue remodeling and fibrosis development. Recently, group 2 innate lymphoid cells (ILC2s) were newly described as central innate mediators of type 2 responses. In particular, by secretion of the cytokines IL-5, IL-9, and IL-13 and the growth factor amphiregulin in response to the release of tissue-derived alarmins, ILC2s have been shown to substantially contribute to both the dismissal of metazoan parasites and the repair of infection-dependent or sterile tissue damage. Conversely, cytokine production by ILC2s emerged as a driving force for tissue remodeling and excessive fibrosis in several organ systems including the lung, liver, and skin. In this review, we discuss how ILC2s are specifically implicated in the body's immune response to different pathogenic infections and how dysregulated ILC2s may promote organ-specific fibrosis.

Indexed as

Disease SusceptibilityHost-Pathogen InteractionsImmunity, InnateAnimalsBiomarkersCommunicable DiseasesCytokinesFibrosisGene Expression RegulationHost-Parasite InteractionsHumansInflammation MediatorsLymphocyte SubsetsOrgan SpecificitySignal TransductionWound HealingBiomarkersCytokinesInflammation MediatorsFibrosisGroup 2 innate lymphoid cellsILC2sInfectious diseasesTissue repair

Identifiers

PMID29623414
OpenAlexW2796222443

What OpenQuestion holds

Textmetadata
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.