Evidence map›Paper›PMID 21624504›Full record

ReviewInternational immunopharmacology2011

The active contribution of Toll-like receptors to allergic airway inflammation.

Keqiang Chen, Yi Xiang, Xiaohong Yao, Ying Liu, Wanghua Gong, Teizo Yoshimura, Ji Ming Wang

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-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

26 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Study from the Signaling Pathways of Four PotentialInternational journal of molecular sciences · 2025
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  10. Review
  11. Review
  12. Article
  13. Review
  14. Expression of Toll-like receptors in nasal epithelium in allergic rhinitis.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2015
    Article
  15. Article
  16. Article
  17. A toll-like receptor 4 (TLR4) variant is associated with asthma severity.International journal of clinical and experimental medicine · 2015
    Article
  18. Article
  19. Article
  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

7 authors at 6 institutions in 2 countries.

Keqiang ChenLaboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, United States.
Yi Xiang
Xiaohong Yao
Ying Liu
Wanghua Gong
Teizo Yoshimura
Ji Ming Wang
Center for Cancer Research · USArmy Medical University · CNFrederick National Laboratory for Cancer Research · USNational Cancer Institute · USRuijin Hospital · CNScience Applications International Corporation (United States) · US

Funding

Role of Formylpeptide Receptors in Host DefenseZIABC010725 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2009 to 2023
$6.3M
The Role of Cellular Receptors Involved in Inflammation and Tumor ProgressionZ01BC010015 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 1996 to 2008
$944k
CCR NIH HHS HHSN261200800001CIntramural NIH HHS Z01 BC010015NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Epithelia lining the respiratory tract represent a major portal of entry for microorganisms and allergens and are equipped with innate and adaptive immune signaling receptors for host protection. These include Toll-like receptors (TLRs) that recognize microbial components and evoke diverse responses in cells of the respiratory system. TLR stimulation by microorganism-derived molecules activates antigen presenting cells, control T helper (Th) 1, Th2, and Th17 immune cell differentiation, cytokine production by mast cells, and activation of eosinophils. It is clear that TLR are involved in the pathophysiology of allergic airway diseases such as asthma. Dendritic cells (DCs), a kind of antigen presenting cells, which play a key role in the induction of allergic airway inflammation, are privileged targets for pathogen associated molecular patterns (PAMPs). During the allergic responses, engagement of TLRs on DCs determines the Th2 polarization of the T cells. TLR signaling in mast cells increases the release of IL-5, and TLR activation of airway epithelial cells forces the generation of proallergic Th2 type of cytokines. Although these responses aim to protect the host, they may also result in inflammatory tissue damage in the airway. Under certain conditions, stimulation of TLRs, in particular, TLR9, may reduce Th2-dependent allergic inflammation by induction of Th1 responses. Therefore, understanding the complex regulatory roles of TLRs in the pathogenesis of allergic airway inflammation should facilitate the development of preventive and therapeutic measures for asthmatic patients.

Indexed as

AnimalsAntigen PresentationAsthmaCell DifferentiationDendritic CellsEosinophilsHumansInterleukin-5Mast CellsMolecular Targeted TherapyRespiratory MucosaSignal TransductionTh1-Th2 BalanceTh2 CellsToll-Like ReceptorsInterleukin-5Toll-Like Receptors

Identifiers

PMID21624504
PMCPMC7398422
OpenAlexW1990037833

What OpenQuestion holds

Textmetadata
LicenceTDM
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.