Evidence map›Paper›PMID 21646293›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Kit (W-sh) mice develop earlier and more severe experimental autoimmune encephalomyelitis due to absence of immune suppression.

Hongmei Li, Bardia Nourbakhsh, Farinaz Safavi, Ke Li, Hui Xu, Melissa Cullimore, Fang Zhou, Guangxian Zhang, Abdolmohamad Rostami

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Mast Cell Biology at Molecular Level: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020
    Review
  4. Review
  5. Mast cells regulate CD4The Journal of allergy and clinical immunology · 2018
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Mast cells contribute to peripheral tolerance and attenuate autoimmune vasculitis.Journal of the American Society of Nephrology : JASN · 2012
    Article
  16. Review
  17. Mast cells: an expanding pathophysiological role from allergy to other disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2012
    Review
  18. Innate immunity in the central nervous system.The Journal of clinical investigation · 2012
    Review
  19. Article
  20. The immunologic revolution: photoimmunology.The Journal of investigative dermatology · 2012
    Review
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 1 institution in 1 country.

Hongmei LiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Bardia Nourbakhsh
Farinaz Safavi
Ke Li
Hui Xu
Melissa Cullimore
Fang Zhou
Guangxian Zhang
Abdolmohamad Rostami
Thomas Jefferson University · US

Funding

The Role of Dendritic Cells in Intravenous ToleranceR01NS048435 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2004 to 2013
$2.9M
NINDS NIH HHS R01 NS048435
6 · The paper itself

Abstract

Mast cells (MCs) have been thought to play a pathogenic role in the development of autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. However, an immunoregulatory function of these cells has recently been suggested. We investigated the role of MCs in EAE using the W(-sh) mouse strain, which is MC deficient. W(-sh) mice developed earlier and more severe clinical and pathological disease with extensive demyelination and inflammation in the CNS. The inflammatory cells were mainly composed of CD4(+) T cells, monocyte/macrophages, neutrophils, and dendritic cells. Compared with wild-type mice, MC-deficient mice exhibited an increased level of MCP-1/CCR2 and CD44 expression on CD4(+) T cells in addition to decreased production of regulatory T cells, IL-4, IL-5, IL-27, and IL-10. We also found that levels of IL-17, IFN-γ, and GM-CSF were significantly increased in peripheral lymphocytes from immunized W(-sh) mice compared with those in peripheral lymphocytes from wild-type mice. Reconstitution of W(-sh) mice downregulated susceptibility to EAE, which correlated with MC recruitment and regulatory T cell activation in the CNS. These findings indicate that responsiveness is not required in the pathogenesis of inflammatory demyelination in the CNS and that, in the absence of MCs, increased MCP-1, CCR2, IL-17, IFN-γ, CD44, and other inflammatory molecules may be responsible for increased severity of EAE.

Indexed as

Severity of Illness IndexAnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleGenetic Predisposition to DiseaseImmune ToleranceInflammationLymphocyte ActivationMast CellsMiceMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsProto-Oncogene Proteins c-kitSpinal CordT-Lymphocytes, RegulatoryMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsProto-Oncogene Proteins c-kit

Identifiers

PMID21646293
PMCPMC4201114
OpenAlexW2098087192

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.