Evidence map›Paper›PMID 25978633›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2015

Peripheral Blood Cells from Patients with Autoimmune Addison's Disease Poorly Respond to Interferons In Vitro, Despite Elevated Serum Levels of Interferon-Inducible Chemokines.

Kine Edvardsen, Trine Bjånesøy, Alexander Hellesen, Lars Breivik, Marit Bakke, Eystein S Husebye, Eirik Bratland

Open access · hybridAbstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Botanically-Derived ΔMolecules (Basel, Switzerland) · 2022
    Article
  4. Review
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  6. Encountering COVID-19 as Endocrinologists.Endocrinology and metabolism (Seoul, Korea) · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. 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

7 authors at 2 institutions in 1 country.

Kine Edvardsen1 Department of Clinical Science, University of Bergen , Bergen, Norway .
Trine Bjånesøy2 Department of Biomedicine, University of Bergen , Bergen, Norway .
Alexander Hellesen1 Department of Clinical Science, University of Bergen , Bergen, Norway .
Lars Breivik1 Department of Clinical Science, University of Bergen , Bergen, Norway .
Marit Bakke2 Department of Biomedicine, University of Bergen , Bergen, Norway .
Eystein S Husebye1 Department of Clinical Science, University of Bergen , Bergen, Norway .
Eirik Bratland1 Department of Clinical Science, University of Bergen , Bergen, Norway .
University of Bergen · NOHaukeland University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune Addison's disease (AAD) is a disorder caused by an immunological attack on the adrenal cortex. The interferon (IFN)-inducible chemokine CXCL10 is elevated in serum of AAD patients, suggesting a peripheral IFN signature. However, CXCL10 can also be induced in adrenocortical cells stimulated with IFNs, cytokines, or microbial components. We therefore investigated whether peripheral blood mononuclear cells (PBMCs) from AAD patients display an enhanced propensity to produce CXCL10 and the related chemokine CXCL9, after stimulation with type I or II IFNs or the IFN inducer poly (I:C). Although serum levels of CXCL10 and CXCL9 were significantly elevated in patients compared with controls, IFN stimulated patient PBMC produced significantly less CXCL10/CXCL9 than control PBMC. Low CXCL10 production was not significantly associated with medication, disease duration, or comorbidities, but the low production of poly (I:C)-induced CXCL10 among patients was associated with an AAD risk allele in the phosphatase nonreceptor type 22 (PTPN22) gene. PBMC levels of total STAT1 and -2, and IFN-induced phosphorylated STAT1 and -2, were not significantly different between patients and controls. We conclude that PBMC from patients with AAD are deficient in their response to IFNs, and that the adrenal cortex itself may be responsible for the increased serum levels of CXCL10.

Indexed as

Addison DiseaseAdultAgedAged, 80 and overCase-Control StudiesChemokine CXCL10Chemokine CXCL9ChemokinesComorbidityEnzyme-Linked Immunosorbent AssayFemaleGenotypeHumansInterferonsLeukocytes, MononuclearMaleChemokine CXCL10Chemokine CXCL9ChemokinesInterferonsPoly I-CProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanSTAT1 Transcription FactorSTAT2 Transcription Factor

Identifiers

PMID25978633
PMCPMC4589105
OpenAlexW2223369677

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.