{'fraction_non_alphanumeric': 0.02478448275862069, 'fraction_numerical': 0.016163793103448277, 'mean_word_length': 5.319727891156463, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The level of B7 homologue 1 expression on brain DC is decisive for CD8 Treg cell recruitment into the CNS during EAE

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.