Evidence map›Paper›PMID 18377768›Full record

ReviewCurrent allergy and asthma reports2008

Toll-like receptors in the respiratory system: their roles in inflammation.

Chiaki Iwamura, Toshinori Nakayama

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current allergy and asthma reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Toll-Like Receptors-2 and -4 in Graves' Disease-Key Players or Bystanders?International journal of molecular sciences · 2019
    Article
  7. Review
  8. Immune Defense Protein Expression in Highly Purified Mouse Lung Epithelial Cells.American journal of respiratory cell and molecular biology · 2016
    Article
  9. Review
  10. A toll-like receptor 4 (TLR4) variant is associated with asthma severity.International journal of clinical and experimental medicine · 2015
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Toll-like receptors in chronic pain.Experimental neurology · 2012
    Review
  18. Review
  19. Lung cancer and Toll-like receptors.Cancer immunology, immunotherapy : CII · 2011
    Review
  20. Maternal signals for progeny prevention against allergy and asthma.Cellular and molecular life sciences : CMLS · 2011
    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

2 authors at 1 institution in 1 country.

Chiaki IwamuraDepartment of Immunology (H3), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Toshinori Nakayama
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic airway inflammation develops in the context of innate immune cells that express Toll-like receptors (TLRs). TLRs recognize microbial components and evoke diverse responses in immune and other respiratory cells through distinct signaling pathways. Bacterial and viral infection in the airway modulates the extent of allergic inflammation. TLR stimulation controls T helper (Th) 1, Th2, and Th17 cell differentiation, cytokine production in mast cells, and activation of eosinophils via direct and indirect pathways. TLR signals in dendritic cells increase expression of major histocompatibility complex proteins and T-cell coreceptors, resulting in greater T-cell activation with Th1 bias. TLR signals in mast cells increase their release of IL-5, and TLR signals in airway epithelial cells enhance airway generation of proallergic cytokines. Although these responses play an important protective role in infection, they may exacerbate allergic inflammation. Under some conditions, TLR stimulation, especially via TLR9, reduces Th2-dependent allergic inflammation through induction of Th1 responses. Therefore, understanding the regulatory role of TLRs in the pathogenesis of allergic airway inflammation may shed light on improving inflammation control in asthmatic patients.

Indexed as

AsthmaCytokinesDendritic CellsEosinophilsHumansHypersensitivityInflammationLymphocyte ActivationMast CellsRespiratory SystemSignal TransductionTh1 CellsTh2 CellsToll-Like ReceptorsCytokinesToll-Like Receptors

Identifiers

PMID18377768
OpenAlexW2002436848

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.