Evidence map›Paper›PMID 22503411›Full record

ArticleJournal of neuroimmunology2012

Antibody to α4 integrin suppresses natural killer cells infiltration in central nervous system in experimental autoimmune encephalomyelitis.

Yan Gan, Ruolan Liu, Wei Wu, Roberto Bomprezzi, Fu-Dong Shi

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroimmunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. The role of CD56Journal of neuroinflammation · 2024
    Review
  6. Natural killer cells in the central nervous system.Cell communication and signaling : CCS · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. NK cell trafficking in health and autoimmunity:a comprehensive review.Clinical reviews in allergy & immunology · 2014
    Review
  16. Review
  17. Impaired learning resulting from respiratory syncytial virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  18. Adhesion molecules in CNS disorders: biomarker and therapeutic targets.CNS & neurological disorders drug targets · 2013
    Review
  19. Article
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 3 institutions in 2 countries.

Yan GanDepartment of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, United States.
Ruolan Liu
Wei Wu
Roberto Bomprezzi
Fu-Dong Shi
Barrow Neurological Institute · USSt. Joseph's Hospital and Medical Center · USTianjin Medical University General Hospital · CN

Funding

NK cells in CNS inflammation and autoimmunityR01AI083294 · NIAID · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI SHI, FU-DONG · 2010 to 2014
$2.0M
NIAID NIH HHS R01 AI083294NIAID NIH HHS R01AI083294
6 · The paper itself

Abstract

Natalizumab inhibits the influx of leukocytes into the central nervous system (CNS) via blockade of alpha-4 subunit of very late activation antigen (VLA)-4. The association of natalizumab therapy with progressive multifocal leukoencephalopathy (PML) suggests a disturbance of CNS immune surveillance in a small percentage of Multiple Sclerosis (MS) patients exposed to the medication. Natural killer (NK) cells are known to play an important role in modulating the evolution of different phases of this lymphocyte mediated disease, and we investigated the effects of natalizumab on the NK cell phenotype and infiltration in the CNS in experimental autoimmune encephalomyelitis (EAE), a murine model of MS. Our data show that both resting (from naïve mice) and activated (from EAE mice) NK cells express high levels of VLA-4, and anti-VLA-4 antibody treatment significantly decreases NK cells frequency in the CNS of EAE mice. Moreover, we find that anti-VLA-4 possibly impairs NK cells migratory potential, since unblocked VLA-4 expression levels were downregulated on those NK cells that penetrate the CNS. These data suggest that treatment with antibody to VLA-4 may alter immune surveillance of the CNS by impacting NK cell functions and might contribute to the understanding of the mechanisms leading to the development of PML in some MS patients.

Indexed as

AnimalsAntibodiesAntigens, CDCell MovementCentral Nervous SystemDisease Models, AnimalDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFemaleFlow CytometryGlycoproteinsIntegrin alpha4Killer Cells, NaturalLeukocytes, MononuclearMiceMice, Inbred C57BLAntibodiesAntigens, CDGlycoproteinsIntegrin alpha4Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID22503411
PMCPMC3351567
OpenAlexW2089521611

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.