Evidence map›Paper›PMID 32290250›Full record

ArticleCells2020

Interleukin 26 Skews Macrophage Polarization Towards M1 Phenotype by Activating cJUN and the NF-κB Pathway.

Yi-Hsuan Lin, Yi-Hsun Wang, Yi-Jen Peng, Feng-Cheng Liu, Gu-Jiun Lin, Shing-Hwa Huang, Huey-Kang Sytwu, Chia-Pi Cheng

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Multifaceted Roles of IL-26 in Physiological and Pathological Conditions.International journal of molecular sciences · 2025
    Review
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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

8 authors at 3 institutions in 1 country.

Yi-Hsuan LinGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, Taiwan.
Yi-Hsun WangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, Taiwan.
Yi-Jen PengDepartment of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Feng-Cheng LiuRheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Gu-Jiun LinDepartment and Graduate Institute of Biology and Anatomy, National Defense Medical Center, Taipei 114, Taiwan.
Shing-Hwa HuangDepartment of General Surgery, En Chu Kong Hospital, New Taipei 237, Taiwan.
Huey-Kang SytwuNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Zhunan 350, Miaoli County, Taiwan.
Chia-Pi ChengGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, Taiwan.
National Defense Medical Center · TWTri-Service General Hospital · TWNational Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 26 (IL-26) is a new member of the IL-10 family that is highly expressed in rheumatoid arthritis (RA). However, the functions of IL-26 produced by macrophages in RA have not been elucidated. In the present work, we evaluated the effects and the mechanisms of IL-26 on M1 and M2 macrophage differentiation. Human or mouse macrophage cells were treated with lipopolysaccharides (LPS), interferon gamma (IFNγ), or IL-4 alone or concurrently treated with IL-26 to monitor M1 or M2 macrophage subtypes. The expression level of M1 or M2 macrophage genes was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The molecular mechanisms of downstream signaling activation during differentiation were investigated by immunoblotting assay. Our results found that IL-26 promoted macrophage cells from CD80

Indexed as

AnimalsCell DifferentiationCell PolarityHumansInterleukinsMacrophage ActivationMacrophagesMiceNF-kappa BPhenotypeProto-Oncogene Proteins c-junRAW 264.7 CellsIL26 protein, humanInterleukinsNF-kappa BProto-Oncogene Proteins c-juninterleukin-26macrophage differentiationrheumatoid arthritis

Identifiers

PMID32290250
PMCPMC7227026
OpenAlexW3015496674

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.