Evidence map›Paper›PMID 30968186›Full record

ReviewSeminars in immunopathology2019

The immunopathology of lung fibrosis: amphiregulin-producing pathogenic memory T helper-2 cells control the airway fibrotic responses by inducing eosinophils to secrete osteopontin.

Kiyoshi Hirahara, Ami Aoki, Yuki Morimoto, Masahiro Kiuchi, Mikiko Okano, Toshinori Nakayama

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Clinical management of checkpoint inhibitor pneumonitis: Focus, challenges, and future directions.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  8. Review
  9. Review
  10. The role of IL-1 family of cytokines and receptors in pathogenesis of COVID-19.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  11. Article
  12. Crosstalk between ILC2s and Th2 CD4Journal of immunology research · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. The Role of CD4Frontiers in immunology · 2021
    Review
  17. Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Kiyoshi HiraharaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. hiraharak@chiba-u.jp.
Ami AokiDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Yuki MorimotoDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Masahiro KiuchiDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Mikiko OkanoDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is defined as excessive deposition of the extracellular matrix (ECM) in the parenchyma of various organs, and sometimes leads to irreversible organ malfunction such as idiopathic pulmonary fibrosis (IPF), a fatal disorder of the lung. Chronic inflammatory stimuli induce fibrotic responses in various organs. Various immune cells, including T helper (Th) cells in the lung, protect the host from different harmful particles, including pathogenic microorganisms. However, the dysregulation of the function of these immune cells in the lung sometimes causes inflammatory diseases, such as lung fibrosis. In this review, we will introduce an outline of the cellular and molecular mechanisms underlying the pathogenic fibrotic responses in the lung. We will also introduce the concept of the "Pathogenic Th population disease induction model," in which unique subpopulations of certain Th cell subsets control the pathology of immune-mediated inflammatory diseases. Finally, we introduce our recent findings, which demonstrate that amphiregulin-producing pathogenic memory Th2 cells control airway fibrosis through the osteopontin produced by inflammatory eosinophils. The identification of this new pathogenic Th cell population supports the concept of "Pathogenic Th population disease induction model", and will provide novel strategies for treating intractable diseases, including lung fibrosis.

Indexed as

AmphiregulinAnimalsBiomarkersCytokinesDisease Models, AnimalDisease SusceptibilityEosinophilsHumansImmunologic MemoryMiceOsteopontinPulmonary FibrosisRespiratory MucosaTh2 CellsT-Lymphocyte SubsetsAmphiregulinBiomarkersCytokinesOsteopontinAmphiregulin-producing pathogenic memory Th2 cellsAsthmaExtracellular matrix (ECM)FibrosisInflammatory eosinophilsOsteopontin“Pathogenic Th population disease induction model”

Identifiers

PMID30968186
OpenAlexW2935727611

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.