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

TitleCaveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis
Authors
Issue Date2016
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
The Journal of Neuroscience, 2016, v. 36 n. 19, p. 5193-5199 How to Cite?
AbstractMultiple 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.
Persistent Identifierhttp://hdl.handle.net/10722/228951
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105

 

DC FieldValueLanguage
dc.contributor.authorWU, H-
dc.contributor.authorDeng, R-
dc.contributor.authorChen, X-
dc.contributor.authorWong, WM-
dc.contributor.authorChen, H-
dc.contributor.authorGao, L-
dc.contributor.authorNi, YC-
dc.contributor.authorWu, W-
dc.contributor.authorShen, J-
dc.date.accessioned2016-08-23T14:08:03Z-
dc.date.available2016-08-23T14:08:03Z-
dc.date.issued2016-
dc.identifier.citationThe Journal of Neuroscience, 2016, v. 36 n. 19, p. 5193-5199-
dc.identifier.issn0270-6474-
dc.identifier.urihttp://hdl.handle.net/10722/228951-
dc.description.abstractMultiple 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.-
dc.languageeng-
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org-
dc.relation.ispartofThe Journal of Neuroscience-
dc.rightsThe Journal of Neuroscience. Copyright © Society for Neuroscience.-
dc.titleCaveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis-
dc.typeArticle-
dc.identifier.emailDeng, R: rxdeng@hku.hk-
dc.identifier.emailChen, X: chenxm@hku.hk-
dc.identifier.emailWong, WM: wmwonga@hku.hk-
dc.identifier.emailChen, H: chenhs@hku.hk-
dc.identifier.emailWu, W: wtwu@hkucc.hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.authorityWu, W=rp00419-
dc.identifier.authorityShen, J=rp00487-
dc.identifier.doi10.1523/JNEUROSCI.3734-15.2016-
dc.identifier.pmid27170118-
dc.identifier.hkuros261525-
dc.identifier.volume36-
dc.identifier.issue19-
dc.identifier.spage5193-
dc.identifier.epage5199-
dc.publisher.placeUnited States-

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