Evidence map›Paper›PMID 26153763›Full record

ArticleMucosal immunology2016

Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

B Lamarthée, F Malard, C Gamonet, C Bossard, M Couturier, J-C Renauld, M Mohty, P Saas, B Gaugler

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In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.2field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  4. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
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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

9 authors at 3 institutions in 2 countries.

B LamarthéeINSERM UMR1098, Besançon, France.
F MalardCentre de Recherche Saint-Antoine, INSERM UMRs938, Paris, France.
C GamonetINSERM UMR1098, Besançon, France.
C BossardEA4273 Biometadys, Faculté de médecine, Université de Nantes, Nantes, France.
M CouturierINSERM UMR1098, Besançon, France.
J-C RenauldLudwig Institute for Cancer Research and Experimental Medicine Unit, Université Catholique de Louvain, Brussels, Belgium.
M MohtyCentre de Recherche Saint-Antoine, INSERM UMRs938, Paris, France.
P SaasINSERM UMR1098, Besançon, France.
B GauglerINSERM UMR1098, Besançon, France.
Inserm · FRCentre Hospitalier Universitaire de Nantes · FRLudwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL-22 and type I IFN in aGVHD, we transplanted recipient mice, either wild-type (WT) or type I IFN receptor deficient (IFNAR(-/-)), with bone marrow cells and WT or IL-22 deficient (IL-22(-/-)) T cells. We observed a decreased GVHD severity in IFNAR(-/-) recipient of IL-22(-/-) T cells, which was associated with a lower level of STAT1 activation and reduced CXCL10 expression in the large intestine. Finally, immunohistochemistry staining of STAT1 performed on gastrointestinal biopsies of 20 transplanted patients showed exacerbated STAT1 activation in gastrointestinal tissues of patients with aGVHD as compared with those without aGVHD. Thus, interfering with both IL-22 and type I IFN signaling may provide a novel approach to limit aGVHD.

Indexed as

Bone Marrow TransplantationAnimalsBone MarrowChemokine CXCL10Gene Expression RegulationGraft vs Host DiseaseHematologic NeoplasmsHumansInterferon Type IInterleukin-22InterleukinsIntestinal MucosaIntestine, LargeMiceMice, Inbred BALB CMice, Inbred C57BLChemokine CXCL10Cxcl10 protein, mouseIfnar1 protein, mouseInterferon Type IInterleukin-22InterleukinsReceptor, Interferon alpha-betaStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID26153763
OpenAlexW2261359868

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.