Evidence map›Paper›PMID 20805418›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Neutralization of IL-9 ameliorates experimental autoimmune encephalomyelitis by decreasing the effector T cell population.

Hongmei Li, Bardia Nourbakhsh, Bogoljub Ciric, Guang-Xian Zhang, Abdolmohamad Rostami

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

66 citing papers in PubMed, 126 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Th9 cells provide protective TB immunity.Frontiers in immunology · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. The World according to IL-9.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  13. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

6 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

5 authors at 1 institution in 1 country.

Hongmei LiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Bardia Nourbakhsh
Bogoljub Ciric
Guang-Xian Zhang
Abdolmohamad Rostami
Thomas Jefferson University · US

Funding

The Role of the TH17 cells in the pathogenesis of EAER01NS046782 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2003 to 2013
$2.7M
NINDS NIH HHS R01 NS046782
6 · The paper itself

Abstract

Multiple sclerosis is a CD4(+) T cell-mediated autoimmune disease affecting the CNS. Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), have been thought to be Th1-mediated diseases. However, recent studies provide strong evidence that the major pathogenic T cell subsets in EAE are Th17 cells. IL-9, a hematopoietic growth factor, is considered to be a mediator of Th17 cells, but the precise mechanisms of its action are largely unknown. The present study was designed to investigate the role of IL-9 in autoimmune demyelination. IL-9 blockade with anti-IL-9 mAb inhibited the development of EAE, reduced the serum levels of IL-17, the CNS mRNA expression of IL-17, IL-6, IFN-γ, and TNF-α, and the myelin oligodendrocyte glycoprotein (MOG)-induced IL-17, IFN-γ secretion of lymphocytes. Furthermore, anti-IL-9 mAb in culture suppressed IL-17 production of MOG-reactive T cells and their potency in adoptive transfer EAE. These findings indicate that the protective effect of IL-9 blockade in EAE was likely mediated via inhibition of the development of MOG peptide-specific T cells, which in turn led to reduced infiltration of T cells into the CNS. Thus, anti-IL-9 mAb treatment may provide an effective therapeutic strategy against autoimmune diseases.

Indexed as

AnimalsAntibodies, MonoclonalCD4-Positive T-LymphocytesCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalGene ExpressionInterleukin-17Interleukin-9MiceMice, Inbred C57BLReverse Transcriptase Polymerase Chain ReactionSpinal CordT-Lymphocyte SubsetsAntibodies, MonoclonalInterleukin-17Interleukin-9

Identifiers

PMID20805418
PMCPMC2978501
OpenAlexW2112334818

What OpenQuestion holds

Textmetadata
LicenceTDM
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.