Evidence map›Paper›PMID 16543475›Full record

ArticleBlood2006

The chemokine CXCL13 is a key molecule in autoimmune myasthenia gravis.

Amel Meraouna, Geraldine Cizeron-Clairac, Rozen Le Panse, Jacky Bismuth, Frederique Truffault, Chantal Tallaksen, Sonia Berrih-Aknin

Abstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Myasthenia gravis and five autoimmune diseases: a bidirectional Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Pooled it
  2. Review
  3. Frontiers in immunology · 2026
    Article
  4. Circulating inflammatory proteins as pathogenic mediators and potential therapeutic targets in myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Myasthenia gravis: the future is here.The Journal of clinical investigation · 2024
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Amel MeraounaCentre National de la Recherche Scientifique-Unité mixte de recherche CNRS-UMR 8162, Institut Paris-Sud Cytokines (IPSC), Université Paris XI, Hôpital Marie Lannelongue, Le Plessis-Robinson, France.
Geraldine Cizeron-Clairac
Rozen Le Panse
Jacky Bismuth
Frederique Truffault
Chantal Tallaksen
Sonia Berrih-Aknin
Centre National de la Recherche Scientifique · FR

Funding

AUTOREACTIVITY TO AChR IN THE THYMUS OF MG PATIENTSR01NS039869 · NINDS · HOPITAL MARIE LANNELONGUE · PI BERRIH-AKNIN, SONIA · 2001 to 2004
$500k
NINDS NIH HHS NS39869NINDS NIH HHS R01 NS039869-03NINDS NIH HHS R01 NS039869-04
6 · The paper itself

Abstract

Myasthenia gravis (MG) is associated with ectopic germinal centers in the thymus. Thymectomy and glucocorticoids are the main treatments but they induce operative risks and side effects, respectively. The aim of this study was to propose new therapies more efficient for MG. We hypothesized that molecules dysregulated in MG thymus and normalized by glucocorticoids may play a key role in thymic pathogenesis. Using gene chip analysis, we identified 88 genes complying with these criteria, the most remarkable being the B-cell chemoattractant (CXCL13). Its expression was increased in thymus and sera of glucocorticoid-untreated patients and decreased in response to treatment in correlation with clinical improvement. Normal B cells were actively chemoattracted by thymic extracts from glucocorticoid-untreated patients, an effect inhibited by anti-CXCL13 antibodies. In the thymus, CXCL13 was preferentially produced by epithelial cells and overproduced by epithelial cells from MG patients. Altogether, our results suggest that a high CXCL13 production by epithelial cells could be responsible for germinal center formation in MG thymus. Furthermore, they show that this gene is a main target of corticotherapy. Thus, new therapies targeting CXCL13 could be of interest for MG and other autoimmune diseases characterized by ectopic germinal center formation.

Indexed as

Adrenal Cortex HormonesAdultCase-Control StudiesChemokine CXCL13Chemokines, CXCEpithelial CellsFemaleGene Expression ProfilingGene Expression RegulationGerminal CenterHumansMyasthenia GravisOligonucleotide Array Sequence AnalysisThymus GlandAdrenal Cortex HormonesChemokine CXCL13Chemokines, CXCCXCL13 protein, human

Identifiers

PMID16543475
PMCPMC1847364
OpenAlexW2046251896

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.