Evidence map›Paper›PMID 20364327›Full record

ArticleMolecular biology reports2011

SIGIRR inhibits toll-like receptor 4, 5, 9-mediated immune responses in human airway epithelial cells.

Chun Zhang, Xueling Wu, Yunfeng Zhao, Zhaoxia Deng, Guisheng Qian

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. SIGIRR: An Orphan Receptor Mediating Anti-inflammatory Actions.Expert reviews in molecular medicine · 2025
    Review
  2. Article
  3. Dominant-Negative Form of SIGIRR: SIGIRRJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Increased ratio of Th17 cells to SIGIRRBiomedical reports · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Interleukin-1alpha and HMGB1 mediate hippocampal dysfunction in SIGIRR-deficient mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

5 authors at 3 institutions in 1 country.

Chun ZhangInstitute of Respiratory Medicine, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, People's Republic of China.
Xueling Wu
Yunfeng Zhao
Zhaoxia Deng
Guisheng Qian
Army Medical University · CNXinqiao Hospital · CNZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human airway epithelial cells (HAEC) may contribute to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) through toll-like receptors (TLRs)-mediated molecular mechanisms. TLRs exist on the surface of HAEC where binding to their cognate ligands initiates airway inflammation. Single immunoglobulin interleukin-1 receptor-related protein (SIGIRR) is a member of the toll-interleukin-1 receptor (TIR) family that can negatively modulate the immune response. We carried out studies to characterize SIGIRR modulation of TLR-mediated immune response in HAEC and to define its mechanisms of action. Following treatment with various concentrations of LPS, flagellin and CpG DNA, the levels of cognate TLRs 4, 5, and 9 were measured in the supernatants of HAEC over-expressing the SIGIRR molecule. Moreover, the interaction of the TLR adaptor myeloid differentiation factor 88 (MyD88) with SIGIRR in response to LPS-, flagellin- and CpG DNA-stimulation was examined by co-immunoprecipitation. The findings from this study revealed that overexpression of SIGIRR in HAEC stimulated by LPS, flagellin or CpG DNA resulted in attenuated production of the inflammatory mediators IL-6 and TNF-α. This attenuation was not the result of decreased expression of TLR4, 5 or 9, but rather a sequestration of MyD88 to the TLRs. In conclusion, SIGIRR can inhibit TLR4, 5, and 9-mediated immune responses in HAEC and may be a valuable therapeutic target for the prevention of ALI/ARDS.

Indexed as

CytokinesEpithelial CellsFlagellinGene Expression RegulationHumansImmunityInflammation MediatorsLigandsLipopolysaccharidesMyeloid Differentiation Factor 88OligodeoxyribonucleotidesProtein BindingProtein TransportReceptors, Interleukin-1Respiratory SystemRNA, MessengerCPG-oligonucleotideCytokinesFlagellinInflammation MediatorsLigandsLipopolysaccharidesMyeloid Differentiation Factor 88OligodeoxyribonucleotidesReceptors, Interleukin-1RNA, MessengerSIGIRR protein, humanTLR4 protein, humanTLR5 protein, humanTLR9 protein, humanToll-Like Receptor 4Toll-Like Receptor 5Toll-Like Receptor 9Toll-Like Receptors

Identifiers

PMID20364327
OpenAlexW1996391716

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.