Evidence map›Paper›PMID 26113417›Full record

Trial reportHaematologica2015

Deregulation of Fas ligand expression as a novel cause of autoimmune lymphoproliferative syndrome-like disease.

Schafiq Nabhani, Sebastian Ginzel, Hagit Miskin, Shoshana Revel-Vilk, Dan Harlev, Bernhard Fleckenstein, Andrea Hönscheid, Prasad T Oommen, Michaela Kuhlen, Ralf Thiele and 4 more

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Cytolytic CD4Frontiers in immunology · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. StabilizedJournal of immunology research · 2017
    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

14 authors at 6 institutions in 2 countries.

Schafiq NabhaniDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Sebastian GinzelDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany Department of Computer Science, Bonn-Rhein-Sieg University of Applied Sciences, Sankt Augustin, Germany.
Hagit MiskinPediatric Hematology Unit, Shaare Zedek Medical Center, Jerusalem, Israel.
Shoshana Revel-VilkDepartment of Pediatric Hematology-Oncology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Dan HarlevPediatric Hematology Unit, Shaare Zedek Medical Center, Jerusalem, Israel.
Bernhard FleckensteinDepartment of Clinical and Molecular Virology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Andrea HönscheidDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Prasad T OommenDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Michaela KuhlenDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Ralf ThieleDepartment of Computer Science, Bonn-Rhein-Sieg University of Applied Sciences, Sankt Augustin, Germany.
Hans-Jürgen LawsDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Arndt BorkhardtDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Polina StepenskyDepartment of Pediatric Hematology-Oncology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Ute FischerDepartment of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany ute.fischer@med.uni-duesseldorf.de.
Düsseldorf University Hospital · DEHeinrich Heine University Düsseldorf · DEHadassah Medical Center · ILShaare Zedek Medical Center · ILFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHochschule Bonn-Rhein-Sieg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune lymphoproliferative syndrome is frequently caused by mutations in genes involved in the Fas death receptor pathway, but for 20-30% of patients the genetic defect is unknown. We observed that treatment of healthy T cells with interleukin-12 induces upregulation of Fas ligand and Fas ligand-dependent apoptosis. Consistently, interleukin-12 could not induce apoptosis in Fas ligand-deficient T cells from patients with autoimmune lymphoproliferative syndrome. We hypothesized that defects in the interleukin-12 signaling pathway may cause a similar phenotype as that caused by mutations of the Fas ligand gene. To test this, we analyzed 20 patients with autoimmune lymphoproliferative syndrome of unknown cause by whole-exome sequencing. We identified a homozygous nonsense mutation (c.698G>A, p.R212*) in the interleukin-12/interleukin-23 receptor-component IL12RB1 in one of these patients. The mutation led to IL12RB1 protein truncation and loss of cell surface expression. Interleukin-12 and -23 signaling was completely abrogated as demonstrated by deficient STAT4 phosphorylation and interferon γ production. Interleukin-12-mediated expression of membrane-bound and soluble Fas ligand was lacking and basal expression was much lower than in healthy controls. The patient presented with the classical symptoms of autoimmune lymphoproliferative syndrome: chronic non-malignant, non-infectious lymphadenopathy, splenomegaly, hepatomegaly, elevated numbers of double-negative T cells, autoimmune cytopenias, and increased levels of vitamin B12 and interleukin-10. Sanger sequencing and whole-exome sequencing excluded the presence of germline or somatic mutations in genes known to be associated with the autoimmune lymphoproliferative syndrome. Our data suggest that deficient regulation of Fas ligand expression by regulators such as the interleukin-12 signaling pathway may be an alternative cause of autoimmune lymphoproliferative syndrome-like disease.

Indexed as

Codon, NonsenseApoptosisAutoimmune Lymphoproliferative SyndromeCaspase 10Caspase 8Cell Line, TransformedFas Ligand Proteinfas ReceptorFemaleGene Expression RegulationHumansInterleukin-12MaleReceptors, Interleukin-12Signal TransductionSTAT4 Transcription FactorCASP10 protein, humanCASP8 protein, humanCaspase 10Caspase 8Codon, NonsenseFASLG protein, humanFas Ligand ProteinFAS protein, humanfas ReceptorIL12RB1 protein, humanInterleukin-12Receptors, Interleukin-12STAT4 protein, humanSTAT4 Transcription Factor

Identifiers

PMID26113417
PMCPMC4800681
OpenAlexW2180327450

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.