Evidence map›Paper›PMID 22043923›Full record

ArticleImmunology2012

CD300a and CD300f differentially regulate the MyD88 and TRIF-mediated TLR signalling pathways through activation of SHP-1 and/or SHP-2 in human monocytic cell lines.

Eun-Ju Kim, Sang-Min Lee, Kyoungho Suk, Won-Ha Lee

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  13. Genome-wide transcriptomic analysis of microglia reveals impaired responses in aged mice after cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
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  14. Antithrombin: An anticoagulant, anti-inflammatory and antibacterial serpin.Journal of thrombosis and haemostasis : JTH · 2020
    Article
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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

4 authors at 1 institution in 1 country.

Eun-Ju KimSchool of Life Sciences and Biotechnology, Kyungpook National University, Daegu, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, Korea.
Sang-Min Lee
Kyoungho Suk
Won-Ha Lee
Kyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD300a, a membrane protein expressed on myeloid lineages and specific subsets of CD4(+) T cells, has been reported to have inhibitory activities in cellular activation. However, the role of CD300a in Toll-like receptor (TLR) -mediated macrophage activation has not been investigated. The human monocytic cell lines THP-1 and U937 were stimulated with various TLR ligands after triggering of CD300a with specific monoclonal antibody. Interestingly, CD300a blocked TLR4-mediated and TLR9-mediated expression of pro-inflammatory mediators without affecting TLR3-mediated events. In contrast, CD300f, another member of the CD300 family, blocked the activation of cells induced by all TLR ligands. A transient transfection assay using luciferase reporter gene under the regulation of nuclear factor-κB binding sites indicated that co-transfection of CD300f blocked reporter expression induced by over-expression of both myeloid differentiation factor 88 (MyD88) and toll-interleukin 1 receptor-domain-containing adapter-inducing interferon-β (TRIF), whereas CD300a blocked only MyD88-induced events. Synthetic peptides representing immunoreceptor tyrosine-based inhibitory motifs of CD300a or CD300f mimicked the differential inhibition patterns of their original molecules. The use of various signalling inhibitors and Western blotting analysis revealed that TLR9/MyD88-mediated signalling was regulated mainly by SH2-containing tyrosine phosphatase 1 (SHP-1), which could be activated by CD300a or CD300f. In contrast, regulation of the TLR3/TRIF-mediated pathway required the combined action of SHP-1 and SHP-2, which could be accomplished by CD300f but not CD300a. These data indicate that CD300a and CD300f regulate the MyD88 and TRIF-mediated TLR signalling pathways through differential activation of SHP-1 and SHP-2.

Indexed as

Adaptor Proteins, Vesicular TransportAntigens, CDCell LineHumansLigandsMacrophage ActivationMonocytesMyeloid Differentiation Factor 88Peptide FragmentsProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, ImmunologicSignal TransductionToll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9Adaptor Proteins, Vesicular TransportAntigens, CDCD300A protein, humanCD300LF protein, humanLigandsMYD88 protein, humanMyeloid Differentiation Factor 88Peptide FragmentsProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6PTPN11 protein, humanPTPN6 protein, humanReceptors, ImmunologicTICAM1 protein, humanTLR3 protein, humanTLR4 protein, humanTLR9 protein, humanToll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9Toll-Like Receptors

Identifiers

PMID22043923
PMCPMC3311045
OpenAlexW2112650005

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.