Evidence map›Paper›PMID 24788601›Full record

ArticlePloS one2014

Potential role of IL-17-producing iNKT cells in type 1 diabetes.

Shamin Li, Claudine Joseph, Chantal Becourt, Jihene Klibi, Sandrine Luce, Daniele Dubois-Laforgue, Etienne Larger, Christian Boitard, Kamel Benlagha

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-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

15 citing papers in PubMed, 28 citations in OpenAlex.

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  15. iNKT and MAIT Cell Alterations in Diabetes.Frontiers in immunology · 2015
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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 6 institutions in 1 country.

Shamin LiUniv Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Paris, France; INSERM UMR1160, Paris, France.
Claudine JosephUniv Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Paris, France; INSERM UMR1160, Paris, France.
Chantal BecourtUniv Paris Descartes, Sorbonne Paris Cité, Institut Cochin, Paris, France; INSERM U1016, Paris, France.
Jihene KlibiDépartement de Bactériologie, Institut Pasteur, Paris, France.
Sandrine LuceUniv Paris Descartes, Sorbonne Paris Cité, Institut Cochin, Paris, France; INSERM U1016, Paris, France.
Daniele Dubois-LaforgueUniv Paris Descartes, Sorbonne Paris Cité, Institut Cochin, Paris, France; INSERM U1016, Paris, France; Service de Diabétologie, Hôtel Dieu, GH Cochin-Hôtel Dieu-Broca, APHP et Univ Paris Descartes, Paris, France.
Etienne LargerUniv Paris Descartes, Sorbonne Paris Cité, Institut Cochin, Paris, France; INSERM U1016, Paris, France; Service de Diabétologie, Hôtel Dieu, GH Cochin-Hôtel Dieu-Broca, APHP et Univ Paris Descartes, Paris, France.
Christian BoitardUniv Paris Descartes, Sorbonne Paris Cité, Institut Cochin, Paris, France; INSERM U1016, Paris, France; Service de Diabétologie, Hôtel Dieu, GH Cochin-Hôtel Dieu-Broca, APHP et Univ Paris Descartes, Paris, France.
Kamel BenlaghaUniv Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Paris, France; INSERM UMR1160, Paris, France.
Université Paris Cité · FRAssistance Publique – Hôpitaux de Paris · FRDélégation Paris 7 · FRInserm · FRInstitut Pasteur · FRSorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We explored in this study the status and potential role of IL-17-producing iNKT cells (iNKT17) in type 1 diabetes (T1D) by analyzing these cells in patients with T1D, and in NOD mice, a mouse model for T1D. Our analysis in mice showed an increase of iNKT17 cells in NOD vs control C57BL/6 mice, partly due to a better survival of these cells in the periphery. We also found a higher frequency of these cells in autoimmune-targeted organs with the occurrence of diabetes, suggesting their implication in the disease development. In humans, though absent in fresh PMBCs, iNKT17 cells are detected in vitro with a higher frequency in T1D patients compared to control subjects in the presence of the proinflammatory cytokine IL-1β, known to contribute to diabetes occurrence. These IL-1β-stimulated iNKT cells from T1D patients keep their potential to produce IFN-γ, a cytokine that drives islet β-cell destruction, but not IL-4, with a reverse picture observed in healthy volunteers. On the whole, our results argue in favour of a potential role of IL-17-producing iNKT cells in T1D and suggest that inflammation in T1D patients could induce a Th1/Th17 cytokine secretion profile in iNKT cells promoting disease development.

Indexed as

AnimalsDiabetes Mellitus, Type 1HumansInterleukin-17Killer Cells, NaturalMiceMice, Inbred C57BLMice, Inbred NODInterleukin-17

Identifiers

PMID24788601
PMCPMC4005752
OpenAlexW2041412135

What OpenQuestion holds

Textmetadata
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.