Evidence map›Paper›PMID 28405609›Full record

ArticleJCI insight2017

Preconditioned mesenchymal stem cells treat myasthenia gravis in a humanized preclinical model.

Muriel Sudres, Marie Maurer, Marieke Robinet, Jacky Bismuth, Frédérique Truffault, Diane Girard, Nadine Dragin, Mohamed Attia, Elie Fadel, Nicola Santelmo and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. 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
2.6field-weighted citation impact, top 10% 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, 31 citations in OpenAlex.

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  15. Thymectomy in Myasthenia Gravis: A Narrative Review.Saudi journal of medicine & medical sciences
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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

13 authors at 7 institutions in 1 country.

Muriel SudresSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Marie MaurerSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Marieke RobinetSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Jacky BismuthSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Frédérique TruffaultSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Diane GirardSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Nadine DraginSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Mohamed AttiaSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Elie FadelCentre Chirurgical Marie Lannelongue, Le Plessis Robinson, France.
Nicola SantelmoHôpital Civil de Strasbourg, Strasbourg, France.
Camille SicsicDepartment of Neurology, Agnes Ginges Center for human Neurogenetics, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Talma BrennerDepartment of Neurology, Agnes Ginges Center for human Neurogenetics, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Sonia Berrih-AkninSorbonne Universités, UPMC Univ Paris 06, Paris, France.
Institut de Myologie · FRAstrophysique, Instrumentation et Modélisation · FRInserm · FRCentre Chirurgical Marie Lannelongue · FRCentre de Recherche en MyologieHôpital Civil, Strasbourg · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) with anti-acetylcholine receptor (AChR) Abs is an autoimmune disease characterized by severe defects in immune regulation and thymic inflammation. Because mesenchymal stem cells (MSCs) display immunomodulatory features, we investigated whether and how in vitro-preconditioned human MSCs (cMSCs) could treat MG disease. We developed a new humanized preclinical model by subcutaneously grafting thymic MG fragments into immunodeficient NSG mice (NSG-MG model). Ninety percent of the animals displayed human anti-AChR Abs in the serum, and 50% of the animals displayed MG-like symptoms that correlated with the loss of AChR at the muscle endplates. Interestingly, each mouse experiment recapitulated the MG features of each patient. We next demonstrated that cMSCs markedly improved MG, reducing the level of anti-AChR Abs in the serum and restoring AChR expression at the muscle endplate. Resting MSCs had a smaller effect. Finally, we showed that the underlying mechanisms involved (a) the inhibition of cell proliferation, (b) the inhibition of B cell-related and costimulatory molecules, and (c) the activation of the complement regulator DAF/CD55. In conclusion, this study shows that a preconditioning step promotes the therapeutic effects of MSCs via combined mechanisms, making cMSCs a promising strategy for treating MG and potentially other autoimmune diseases.

Indexed as

AdolescentAdultAnimalsAntibodies, MonoclonalB-LymphocytesChildDisease Models, AnimalFemaleHeterograftsHumansMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, Inbred NODMice, SCIDAntibodies, MonoclonalReceptors, Cholinergic

Identifiers

PMID28405609
PMCPMC5374074
OpenAlexW2604123086

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.