Evidence map›Paper›PMID 23258953›Full record

ReviewMediators of inflammation2012

CC-chemokine CCL15 expression and possible implications for the pathogenesis of IgE-related severe asthma.

Yasuo Shimizu, Kunio Dobashi

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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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

2 authors at 2 institutions in 1 country.

Yasuo ShimizuDepartment of Pulmonary Medicine, Maebashi Red Cross Hospital, 3-21-36 Asahi-Cho, Gunma, Maebashi 371-0014, Japan. yasuos@med.gunma-u.ac.jp
Kunio Dobashi
Gunma University · JPMaebashi Red Cross Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway inflammation is accompanied by infiltration of inflammatory cells and an abnormal response of airway smooth muscle. These cells secrete chemokines and express the cell surface chemokine receptors that play an important role in the migration and degranulation of inflammatory cells. Omalizumab is a monoclonal antibody directed against immunoglobulin E, and its blocking of IgE signaling not only reduces inflammatory cell infiltration mediated by the Th2 immune response but also inhibits other immune responses. The chemokine CCL15 is influenced by omalizumab, and the source of CCL15 has been reported to be airway smooth muscle cells and basophils. CCL15 binds to its receptor CCR1, which has been reported to be expressed by various inflammatory cells and also by airway smooth muscle cells. Therefore, CCL15/CCR1 signaling could be a target for the treatment of asthma. We review the role of CCL15 in the pathogenesis of asthma and also discuss the influence of IgE-mediated immunomodulation via CCL15 and its receptor CCR1.

Indexed as

Antibodies, Anti-IdiotypicAntibodies, Monoclonal, HumanizedAsthmaChemokines, CCClinical Trials as TopicHumansImmunoglobulin EInterferon-gammaMacrophage Inflammatory ProteinsOmalizumabReceptors, CCR1RNA, MessengerSignal TransductionTumor Necrosis Factor-alphaAntibodies, Anti-IdiotypicAntibodies, Monoclonal, HumanizedCCL15 protein, humanCCR1 protein, humanChemokines, CCImmunoglobulin EInterferon-gammaMacrophage Inflammatory ProteinsOmalizumabReceptors, CCR1RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID23258953
PMCPMC3508751
OpenAlexW2026644297

What OpenQuestion holds

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LicenceCC BY
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.