Epstein-Barr virus infection of human brain microvessel endothelial cells: A novel role in multiple sclerosis

被引：56

作者：

Casiraghi, Costanza ^{[1
]}

Dorovini-Zis, Katerina ^{[2
,3
]}

Horwitz, Marc S. ^{[1
]}

机构：

[1] Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC V6T 1Z3, Canada

[2] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada

[3] Vancouver Gen Hosp, Vancouver, BC V5Z 1M9, Canada

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2011年 / 230卷 / 1-2期

关键词：

Multiple sclerosis; Epstein-Barr virus; Human brain microvessel endothelial cells; Blood-brain barrier; Endothelial cells; Inflammation; EPITHELIAL-CELLS; BETA-CHEMOKINES; MIGRATION; ADHESION; CYTOMEGALOVIRUS; ASSOCIATION; LYMPHOCYTES; IMMUNOLOGY; EXPRESSION; FEATURES;

D O I：

10.1016/j.jneuroim.2010.08.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：173 / 177

页数：5

共 33 条

[1] The Epstein-Barr virus-encoded LMP2A and LMP2B proteins promote epithelial cell spreading and motility [J].

Allen, MD ;

Young, LS ;

Dawson, CW .

JOURNAL OF VIROLOGY, 2005, 79 (03) :1789-1802

[2] Environmental risk factors for multiple sclerosis. Part I: The role of infection [J].

Ascherio, Alberto ;

Munger, Kassandra L. .

ANNALS OF NEUROLOGY, 2007, 61 (04) :288-299

[3] Systemic granulomatous arteritis associated with Epstein-Barr virus infection [J].

Ban, S ;

Goto, Y ;

Kamada, K ;

Takahama, M ;

Watanabe, H ;

Iwahori, T ;

Takeuchi, H .

VIRCHOWS ARCHIV, 1999, 434 (03) :249-254

[4] Molecular virology of Epstein-Barr virus [J].

Bornkamm, GW ;

Hammerschmidt, W .

PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2001, 356 (1408) :437-459

[5]

Brabb T, 1997, J IMMUNOL, V159, P497

[6] Regulation of CCL2 and CCL3 expression in human brain endothelial cells by cytokines and lipopolysaccharide [J].

Chui, Ray ;

Dorovini-Zis, Katerina .

JOURNAL OF NEUROINFLAMMATION, 2010, 7

[7] The adhesion molecule ICAM-1 and its regulation in relation with the blood-brain barrier [J].

Dietrich, JB .

JOURNAL OF NEUROIMMUNOLOGY, 2002, 128 (1-2) :58-68

[8]

DOROVINIZIS K, 1991, LAB INVEST, V64, P425

[9] Epstein-Barr virus B95.8 produced in 293 cells shows marked tropism for differentiated primary epithelial cells and reveals interindividual variation in susceptibility to viral infection [J].

Feederle, Regina ;

Neuhierl, Bernhard ;

Bannert, Helmut ;

Geletneky, Karsten ;

Shannon-Lowe, Claire ;

Delecluse, Henri-Jacques .

INTERNATIONAL JOURNAL OF CANCER, 2007, 121 (03) :588-594

[10] Epstein-Barr virus modulates 5-lipoxygenase product synthesis in human peripheral blood mononuclear cells [J].

Gosselin, J ;

Borgeat, P .

BLOOD, 1997, 89 (06) :2122-2130

← 1 2 3 4 →