Evidence map›Paper›PMID 27445435›Full record

ArticleMediators of inflammation2016

Elevated Plasma Level of Interferon-λ1 in Chronic Spontaneous Urticaria: Upregulated Expression in CD8(+) and Epithelial Cells and Induction of Inflammatory Cell Accumulation.

S F Wang, X Q Gao, Y N Xu, D N Li, H Y Wang, S H He

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. The Dynamics of the Skin's Immune System.International journal of molecular sciences · 2019
    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

6 authors at 3 institutions in 1 country.

S F WangAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China; Department of Dentistry, The Second Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
X Q GaoDepartment of Dentistry, The Second Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Y N XuAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
D N LiAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
H Y WangAllergy and Inflammation Research Institute, The Key Immunopathology Laboratory of Guangdong Province, Shantou University Medical College, Shantou 515031, China.
S H HeAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.ORCID 0000-0003-4760-4816
First Affiliated Hospital of Liaoning Medical University · CNJinzhou Medical University · CNShantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon- (IFN-) λ1 is regarded as a potent bio-active molecule in innate immunity. However, little is known about its role in chronic spontaneous urticaria (CSU). We therefore investigated expression of IFN-λ1 in CSU, its cellular location, and its influence on inflammatory cell accumulation by using flow cytometry analysis, skin tissue dispersion, immunohistochemical stain, and a mouse peritoneal inflammation model. The results showed that level of IFN-λ1 was 2.0-fold higher in plasma of the patients with CSU than the level in healthy control (HC) subjects. Among leukocytes examined, only CD8(+) T cells expressed more IFN-λ1 in CSU blood. Double labeling immunohistochemical staining revealed that IFN-λ1(+) inflammatory cells such as mast cells, eosinophils, B cells, neutrophils, and macrophages were mainly located in dermis, whereas epidermis tissue highly expressed IFN-λ1. IFN-λ1 induced a dose-dependent increase in number of eosinophils, lymphocytes, mast cells, macrophages, and neutrophils in the peritoneum of mice at 6 h following injection, which was inhibited by pretreatment of the animals with anti-intercellular adhesion molecule- (ICAM-) 1 and/or anti-L-selectin antibodies. In conclusion, IFN-λ1 is likely to play a role in the pathogenesis of CSU. Blocking IFN-λ1 production may help to reduce the accumulation of inflammatory cells in the involved CSU skin.

Indexed as

AnimalsCD8-Positive T-LymphocytesCytokinesEpithelial CellsFlow CytometryHumansInterferon-gammaInterferon LambdaInterferonsInterleukin-10Interleukin-4InterleukinsLeukocytesMaleMice, Inbred BALB CThymic Stromal LymphopoietinCytokinesInterferon-gammaInterferon Lambdainterferon-lambda, humaninterferon-lambda protein, mouseInterferonsInterleukin-10Interleukin-4InterleukinsThymic Stromal Lymphopoietin

Identifiers

PMID27445435
PMCPMC4944067
OpenAlexW2474670986

What OpenQuestion holds

Textmetadata
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.