Evidence map›Paper›PMID 25880788›Full record

ArticleClinical and experimental immunology2015

Defective trained immunity in patients with STAT-1-dependent chronic mucocutaneaous candidiasis.

D C Ifrim, J Quintin, L Meerstein-Kessel, T S Plantinga, L A B Joosten, J W M van der Meer, F L van de Veerdonk, M G Netea

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  14. Identification of aPathogens (Basel, Switzerland) · 2020
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  15. On Commensalism ofJournal of fungi (Basel, Switzerland) · 2020
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  19. Interferon stimulation creates chromatin marks and establishes transcriptional memory.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Cutting Edge:Journal of immunology (Baltimore, Md. : 1950) · 2018
    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

8 authors at 2 institutions in 1 country.

D C IfrimDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
J QuintinDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
L Meerstein-KesselDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
T S PlantingaDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
L A B JoostenDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
J W M van der MeerDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
F L van de VeerdonkDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
M G NeteaDepartment of Internal Medicine, Radboud University Nijmegen Medical Centre and Radboud Center for Infectious Diseases (RCI), Nijmegen, the Netherlands.
Radboud University Nijmegen · NLRadboud University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with signal transducer and activator of transcription-1 (STAT1)-dependent chronic mucocutaneous candidiasis (CMC) and patients with STAT3-dependent hyper-immunoglobulin (Ig)E syndrome (HIES) display defects in T helper type 17 (Th17) cytokine production capacity. Despite this similar immune defect in Th17 function, they show important differences in the type of infections to which they are susceptible. Recently, our group reported differential regulation of STAT-1 and STAT-3 transcription factors during epigenetic reprogramming of trained immunity, an important host defence mechanism based on innate immune memory. We therefore hypothesized that STAT1 and STAT3 defects have different effects on trained immunity, and this may partly explain the differences between CMC and HIES regarding the susceptibility to infections. Indeed, while trained immunity was normally induced in cells isolated from patients with HIES, the induction of innate training was defective in CMC patients. This defect was specific for training with Candida albicans, the main pathogen encountered in CMC, and it involved a type II interferon-dependent mechanism. These findings describe the role of STAT-1 for the induction of trained immunity, and may contribute to the understanding of the differences in susceptibility to infection between CMC and HIES patients. This study could also provide directions for personalized immunotherapy in patients suffering from these immunodeficiencies.

Indexed as

beta-GlucansCandida albicansCandidiasis, Chronic MucocutaneousCells, CulturedEnzyme-Linked Immunosorbent AssayHost-Pathogen InteractionsHumansInterferon-gammaInterleukin-17Interleukin-6Job SyndromeLeukocytes, MononuclearLipopolysaccharidesMutationSTAT1 Transcription FactorSTAT3 Transcription Factorbeta-GlucansInterferon-gammaInterleukin-17Interleukin-6LipopolysaccharidesSTAT1 Transcription FactorSTAT3 Transcription FactorTumor Necrosis Factor-alphaCMCHIEStrained immunity

Identifiers

PMID25880788
PMCPMC4557379
OpenAlexW2160446572

What OpenQuestion holds

Textmetadata
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.