Evidence map›Paper›PMID 28665693›Full record

ArticleAmerican journal of respiratory cell and molecular biology2017

Critical Role of IRAK-M in Regulating Antigen-Induced Airway Inflammation.

Mingqiang Zhang, Wei Chen, Weixun Zhou, Yan Bai, Jinming Gao

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 37 citations in OpenAlex.

  1. Inhibiting METTL3 in macrophages alleviates colitis by enhancing M2 polarization via upregulating IRAKM.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
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

5 authors at 3 institutions in 3 countries.

Mingqiang ZhangDepartments of 1 Respiratory Diseases.
Wei Chen2 Cardiology, and.
Weixun Zhou3 Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Yan Bai4 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Jinming GaoDepartments of 1 Respiratory Diseases.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNBrigham and Women's Hospital · USInstitute of Cardiology · PL

Funding

Cholinergic hyperinnernation in early life regulates long-term airway reactivityK08HL135443 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BAI, YAN · 2017 to 2021
$861k
6 · The paper itself

Abstract

Asthma is an airway epithelium disorder involving allergic lung inflammation. IL-1 receptor-associated kinase M (IRAK-M) is a negative regulator of Toll-like receptor (TLR) signaling on airway epithelial cells and macrophages, and it is known to limit the overproduction of cytokines during the inflammatory process. However, the direct role of IRAK-M in asthma pathogenesis is unclear. In the present study, we found a significant elevation of IRAK-M expression in mouse lungs after ovalbumin (OVA) exposure. Compared with wild-type mice, IRAK-M knockout (KO) mice responded to OVA challenge with significantly worse infiltration of airway inflammatory cells, greater airway responsiveness, higher proinflammatory cytokine levels in lung homogenates, and more prominent T-helper cell type 2 (Th2) and Th17 deviation. OVA exposure also induced higher activities of dendritic cells (DCs) and macrophages from IRAK-M KO mouse lungs. Furthermore, adoptive transfer of either IRAK-M KO bone-marrow-derived DCs or macrophages into wild-type mice aggravated OVA-induced airway inflammation. In vitro experiments showed that IRAK-M KO naive CD4

Indexed as

Adoptive TransferAnimalsAsthmaDendritic CellsInflammationInterleukin-1 Receptor-Associated KinasesLungMiceMice, KnockoutOvalbuminTh2 CellsInterleukin-1 Receptor-Associated KinasesIrak3 protein, mouseOvalbuminasthmadendritic cellsIRAK-MmacrophagesT cell subsets

Identifiers

PMID28665693
PMCPMC6943878
OpenAlexW2729880558

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.