Evidence map›Paper›PMID 26771137›Full record

ArticleOncotarget2016

Novel CXCL13 transgenic mouse: inflammation drives pathogenic effect of CXCL13 in experimental myasthenia gravis.

Julia Miriam Weiss, Marieke Robinet, Revital Aricha, Perrine Cufi, Bérengère Villeret, Frida Lantner, Idit Shachar, Sara Fuchs, Miriam C Souroujon, Sonia Berrih-Aknin and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

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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

11 authors at 6 institutions in 2 countries.

Julia Miriam WeissINSERM U974, Paris, France.
Marieke RobinetINSERM U974, Paris, France.
Revital ArichaDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Perrine CufiINSERM U974, Paris, France.
Bérengère VilleretINSERM U974, Paris, France.
Frida LantnerDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Idit ShacharDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Sara FuchsDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Miriam C SouroujonOpen University of Israel, Raanana, Israel.
Sonia Berrih-AkninINSERM U974, Paris, France.
Rozen Le PanseINSERM U974, Paris, France.
Weizmann Institute of Science · ILCentre de Recherche en MyologieCentre National de la Recherche Scientifique · FRInstitut de Myologie · FROpen University of Israel · ILSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal overexpression of CXCL13 is observed in many inflamed tissues and in particular in autoimmune diseases. Myasthenia gravis (MG) is a neuromuscular disease mainly mediated by anti-acetylcholine receptor autoantibodies. Thymic hyperplasia characterized by ectopic germinal centers (GCs) is a common feature in MG and is correlated with high levels of anti-AChR antibodies. We previously showed that the B-cell chemoattractant, CXCL13 is overexpressed by thymic epithelial cells in MG patients. We hypothesized that abnormal CXCL13 expression by the thymic epithelium triggered B-cell recruitment in MG. We therefore created a novel transgenic (Tg) mouse with a keratin 5 driven CXCL13 expression. The thymus of Tg mice overexpressed CXCL13 but did not trigger B-cell recruitment. However, in inflammatory conditions, induced by Poly(I:C), B cells strongly migrated to the thymus. Tg mice were also more susceptible to experimental autoimmune MG (EAMG) with stronger clinical signs, higher titers of anti-AChR antibodies, increased thymic B cells, and the development of germinal center-like structures. Consequently, this mouse model finally mimics the thymic pathology observed in human MG. Our data also demonstrated that inflammation is mandatory to reveal CXCL13 ability to recruit B cells and to induce tertiary lymphoid organ development.

Indexed as

AnimalsB-LymphocytesCells, CulturedChemokine CXCL13Epithelial CellsFemaleFlow CytometryGerminal CenterHumansImmunoenzyme TechniquesInflammationMaleMiceMice, Inbred C57BLMice, TransgenicMyasthenia Gravis, Autoimmune, ExperimentalChemokine CXCL13Cxcl13 protein, mouseRNA, MessengerautoimmunityB cellschemokineCXCL13-CXCR5Immune responseImmunityImmunology and Microbiology Sectionthymus

Identifiers

PMID26771137
PMCPMC4884937
OpenAlexW2295548105

What OpenQuestion holds

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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.