Evidence map›Paper›PMID 31949260›Full record

ArticleScientific reports2020

Enhanced STAT3 phosphorylation and PD-L1 expression in myeloid dendritic cells indicate impaired IL-27Ralpha signaling in type 1 diabetes.

Z Parackova, P Vrabcova, I Zentsova, J Kayserova, I Richtrova, L Sojka, K Stechova, Z Sumnik, A Sediva

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Article
  3. Role of Interleukins in Type 1 and Type 2 Diabetes.Diagnostics (Basel, Switzerland) · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. IL-27: An endogenous constitutive repressor of human monocytes.Clinical immunology (Orlando, Fla.) · 2020
    Article
  14. IL-27 Regulated CD4Frontiers in immunology · 2020
    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

9 authors at 2 institutions in 1 country.

Z ParackovaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic. zuzana.parackova@fnmotol.cz.
P VrabcovaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
I ZentsovaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
J KayserovaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
I RichtrovaSotio, A. S., Prague, Czech Republic.
L SojkaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
K StechovaDepartment of Internal Medicine, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
Z SumnikDepartment of Pediatrics, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
A SedivaDepartment of Immunology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
Charles University · CZSotio (Czechia) · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 27 (IL-27), a member of the IL-12 family, is important for T cell differentiation; however, little is known about its effect on dendritic cells (DCs). IL-27 can activate multiple signaling cascades, including the JAK/STAT pathway, and depending on the setting it can both promote and antagonize inflammatory responses. An anti-inflammatory function of IL-27 has been reported in several autoimmune diseases; however, in type 1 diabetes (T1D), an autoimmune disease where autoreactive cytotoxic T cells attack insulin-producing beta cells, IL-27 has been shown to have a dual role and contradictory effects. Here, we show impaired IL-27 signaling in a large cohort of T1D patients (n = 51) compared to age- and gender-matched healthy donors. Increased expression of the IL-27 receptor subunit IL-27Ralpha mRNA in purified myeloid DCs (mDCs), detected by gene expression microarrays was mirrored by enhanced signal transduction in T1D mDCs in response to IL-27 stimulation. Higher STAT phosphorylation in T1D patients was also accompanied by elevated expression of the inhibitory molecules PD-L1, PD-L2 and PD-1, which may suggest not only immunomodulatory mechanisms of IL-27 in T1D but also a compensatory effort of T1D dendritic cells against the ongoing inflammation.

Indexed as

Signal TransductionAdultAgedB7-H1 AntigenCase-Control StudiesDendritic CellsDiabetes Mellitus, Type 1FemaleGene Expression ProfilingHumansInterleukinsMaleMiddle AgedOligonucleotide Array Sequence AnalysisPhosphorylationReceptors, InterleukinB7-H1 AntigenCD274 protein, humanIL27RA protein, humanInterleukinsMYDGF protein, humanReceptors, InterleukinSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID31949260
PMCPMC6965661
OpenAlexW2999245349

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.