1887

Abstract

After intracerebral inoculation of Borna disease virus (BDV), Lewis rats develop a persistent infection of the central nervous system which is pathohistologically represented by perivascular encephalitic lesions predominantly in the grey matter. In previous studies it has been shown that a cell-mediated immune response causes Borna disease (BD). In order to define further the immune cell responsible for this immunopathological disease, a BDV-specific T cell line, NM1, was established and cultured . Phenotypically this T cell line was characterized by cytofluorometry as CD4-positive (CD4). Proliferation assays with syngeneic and allogeneic antigen-presenting cells, and blocking experiments with monoclonal antibodies, revealed major histocompatibility complex class II antigens to be restriction elements. After passive transfer of this virus-specific CD4 T cell into immunosuppressed BDV-infected recipients, full-blown disease could be induced. Immunohistological examination of the cells involved in perivascular inflammatory infiltrates in BDV-infected rats and in recipients of the NM1 T cell line revealed a dominance of macrophages and CD4 T cells. The presence of these cells in encephalitic lesions strongly suggests a delayed type of hypersensitivity reaction as the pathogenetic mechanism of BD.

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/content/journal/jgv/10.1099/0022-1317-71-11-2565
1990-11-01
2019-11-13
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http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-71-11-2565
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