Evidence map›Paper›PMID 27170118›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Caveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis.

Hao Wu, Ruixia Deng, Xingmiao Chen, Waiman Connie Wong, Hansen Chen, Lei Gao, Yichu Nie, Wutian Wu, Jiangang Shen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Cyclodextrin Inhibits Caveolin-1 to Regulate CD4Journal of immunology research · 2026
    Article
  4. Revolutionizing Autoimmune Research: The Role of Caveolin-1.Immunity, inflammation and disease · 2025
    Review
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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

9 authors at 4 institutions in 2 countries.

Hao WuSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China.
Ruixia DengSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China.
Xingmiao ChenSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China.
Waiman Connie WongSchool of Biomedical Science, University of Hong Kong, Hong Kong SAR, China.
Hansen ChenSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China.
Lei GaoSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0002-2705-1989
Yichu NieGuangzhou Quality R&D Center of Traditional Chinese Medicine, School of Life Science, Sun Yat-sen University, Guangzhou, 510275, China.
Wutian WuSchool of Biomedical Science, University of Hong Kong, Hong Kong SAR, China, State Key Laboratory of Brain and Cognitive Sciences, University of Hong Kong, Hong Kong SAR, China, and Joint Laboratory for CNS Regeneration, Jinan University and University of Hong Kong, GHM Institute of CNS Regeneration, Jinan University, Guangzhou, 510632, China shenjg@hku.hk wtwu@hku.hk.
Jiangang ShenSchool of Chinese Medicine, University of Hong Kong, Hong Kong SAR, China, shenjg@hku.hk wtwu@hku.hk.
Chinese University of Hong Kong · HKEducation University of Hong Kong · HKJinan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledMultiple sclerosis (MS) is a progressive autoimmune disease of the CNS with its underlying mechanisms not fully understood. In the present study, we tested the hypothesis that caveolin-1, a major membrane scaffolding protein, plays a critical role in the pathogenesis of experimental autoimmune encephalomyelitis, a laboratory murine model of MS. We found increased expression of caveolin-1 in serum and spinal cord tissues in association with disease incidence and severity in wild-type mice with active encephalomyelitis. After immunization, Cav-1 knock-out mice showed remarkable disease resistance with decreased incidence and clinical symptoms. Furthermore, Cav-1 knock-out mice had alleviated encephalitogenic T cells trafficking into the CNS with decreased expressions of adhesion molecules ICAM-1 and VCAM-1 within the lesions. In agreement with in vivo studies, in vitro knockdown of caveolin-1 compromised the upregulation of ICAM-1 in endothelial cells, leading to the amelioration of the transendothelial migration of pathogenic TH1 and TH17 cells. Together, those results indicate that caveolin-1 serves as an active modulator of CNS-directed lymphocyte trafficking and could be a therapeutic target for neuroinflammatory diseases, such as multiple sclerosis. SIGNIFICANCE STATEMENT: The hallmark feature of neuroinflammatory diseases is the massive infiltrations of encephalitogenic leukocytes into the CNS parenchyma, a process that remains largely unclear. Our study demonstrates the critical contribution of caveolin-1 to encephalomyelitis pathogenesis and CNS-directed lymphocyte trafficking by modulation of adhesion molecules ICAM-1 and VCAM-1, highlighting the pathological involvement of caveolin-1 in neuroinflammatory diseases.

Indexed as

Transendothelial and Transepithelial MigrationAnimalsCaveolin 1Cells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFemaleIntercellular Adhesion Molecule-1MiceMice, Inbred C57BLSpinal CordT-LymphocytesVascular Cell Adhesion Molecule-1Caveolin 1Intercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1caveolin-1experimental autoimmune encephalomyelitisICAM-1lymphocyte traffickingVCAM-1

Identifiers

PMID27170118
PMCPMC6601805
OpenAlexW2390751165

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.