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Expression and function of the costimulatory molecules B7-1 (CD80) and B7-2 (CD86) in an in vitro model of the human blood--brain barrier.

Authors
  • Omari, K I
  • Dorovini-Zis, K
Type
Published Article
Journal
Journal of Neuroimmunology
Publisher
Elsevier
Publication Date
Feb 01, 2001
Volume
113
Issue
1
Pages
129–141
Identifiers
PMID: 11137584
Source
Medline
License
Unknown

Abstract

The interaction of B7 molecules with their ligand provides important accessory signals for optimal T cell activation and proliferation. In this study the in vitro expression of B7-1 and B7-2 by human brain microvessel endothelial cells (HBMEC) was investigated by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry. In addition, the contribution of B7 molecules to T cell proliferation on cerebral endothelial cells was studied by coincubating purified CD4+ T cells with resting or cytokine activated HBMEC. Untreated cultures constitutively expressed B7-2 RNA and surface protein, but lacked B7-1 expression. Treatment with TNF-alpha and IFN-gamma upregulated B7-2 and induced de novo expression of B7-1. Monoclonal blocking antibodies to B7-1 or B7-2 and human CTLA-4Ig chimeric protein significantly reduced the ability of HBMEC to support alpha-CD3-induced proliferation of CD4+ T lymphocytes. Expression of B7 glycoproteins and the ability to provide secondary signals for T cell proliferation suggest a potential role of the human cerebral endothelium in T cell activation during the early stages of central nervous system inflammation.

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