Evidence map›Paper›PMID 25938558›Full record

ArticleThe Journal of investigative dermatology2015

Inhibition of EGFR Tyrosine Kinase by Erlotinib Prevents Sclerodermatous Graft-Versus-Host Disease in a Mouse Model.

Florence Morin, Niloufar Kavian, Wioleta Marut, Christiane Chéreau, Olivier Cerles, Philippe Grange, Bernard Weill, Carole Nicco, Frédéric Batteux

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Targeting Cytokines in GVHD Therapy.Journal of immunology research and therapy · 2017
    Article
  9. October 2015 Snapshot Dx Quiz: Linking Science to Patient Care.The Journal of investigative dermatology · 2015
    Article
  10. Review
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 5 institutions in 1 country.

Florence MorinINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France; Laboratoire d'Immunologie biologique, Hôpital Cochin, AP-HP, Paris, France.
Niloufar KavianINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France; Laboratoire d'Immunologie biologique, Hôpital Cochin, AP-HP, Paris, France.
Wioleta MarutINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
Christiane ChéreauINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
Olivier CerlesINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
Philippe GrangeINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
Bernard WeillINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France; Laboratoire d'Immunologie biologique, Hôpital Cochin, AP-HP, Paris, France.
Carole NiccoINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France.
Frédéric BatteuxINSERM U 1016, Institut Cochin, Université Paris Descartes Sorbonne Paris Cité, Faculté de Médecine, Paris, France; Laboratoire d'Immunologie biologique, Hôpital Cochin, AP-HP, Paris, France. Electronic address: frederic.batteux@cch.aphp.fr.
Inserm · FRInstitut Cochin · FRDélégation Paris 5 · FRHôpital Cochin · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic graft-versus-host disease (GVHD) follows allogeneic hematopoietic stem cell transplantation. It results from alloreactive processes induced by minor histocompatibility antigen incompatibilities leading to the activation of CD4 T cells and the development of fibrosis and inflammation of the skin and visceral organs and autoimmunity that resemble systemic sclerosis. EGFR is a ubiquitous cell receptor deeply involved in cell proliferation, differentiation, and motility. EGFR has recently been implicated in autoimmune and fibrotic diseases. Therefore, we tested whether Erlotinib, an EGFR tyrosine kinase inhibitor, can prevent sclerodermatous GVHD (Scl-GVHD). Scl-GVHD was induced in BALB/c mice by B10.D2 bone marrow and spleen cell transplantation. Transplanted mice displayed severe clinical symptoms including alopecia, fibrosis of the skin and visceral organs, vasculitis, and diarrhea. The symptoms were reversed in mice treated with Erlotinib. These beneficial effects were mediated by the decreased production of activated/memory CD4(+) T cells and the reduction in T-cell infiltration of the skin and visceral organs along with a decrease in IFN-γ and IL-13 production and autoimmune B-cell activation. The improvement provided by Erlotinib in the mouse model of Scl-GVHD supplies a rationale for the evaluation of Erlotinib in the management of patients affected by chronic GVHD.

Indexed as

AllograftsAnalysis of VarianceAnimalsBiopsy, NeedleBlotting, WesternCD4-Positive T-LymphocytesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayErlotinib HydrochlorideFemaleFlow CytometryGraft vs Host DiseaseHematopoietic Stem Cell TransplantationImmunohistochemistryInterferon-gammaInterleukin-13Erlotinib HydrochlorideInterferon-gammaInterleukin-13Protein-Tyrosine Kinases

Identifiers

PMID25938558
OpenAlexW1548083421

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.