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pubmed:abstractText |
DC in the CNS have emerged as the major rate-limiting factor for immune invasion and subsequent neuroinflammation during EAE. The mechanism of how this is regulated by brain-localized DC remains unknown. Here, we describe the ability of brain-localized DC expressing B7-H1 molecules to recruit CD8(+) T cells to the site of inflammation. Using intracerebral microinjections of B7-homologue 1-deficient DC, we demonstrate a substantial brain infiltration of CD8(+) T cells displaying a regulatory phenotype (CD122(+)) and function, resulting in a decrease of EAE peak clinical values. The recruitment of regulatory-type CD8(+) T cells into the CNS and the role of brain DC expressing B7-homologue 1 molecules in this process open up the possibility of DC-targeted therapeutic manipulation of neuroinflammatory diseases.
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