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• W1520697345 abstract "The human disease post vaccination (or acute disseminated) encephalomyelitis (ADEM) and its animal counterpart experimental autoimmune encephalomyelitis (EAE) demonstrate that the CNS can be the selective target of a self-antigen directed immune response. These disorders are dependent on systemic CD4+ T cell sensitization to CNS antigens. In contrast to ADEM, the human disorder multiple sclerosis (MS), also postulated to reflect CNS directed immune responses, is characterized by its recurrent and or progressive disease course. The above clinical disorders raise issues regarding the role that resident cells of the CNS play in regulating CNS directed immune responses, under physiologic and pathologic conditions. Such participation could occur at the level of the blood brain barrier (BBB) and/or within the parenchyma of the CNS. BBB-lymphocyte interaction-the molecular events that regulate lymphocyte access to the CNS include those involved in adhesion, chemoattraction, and migration through the cellular and extracellular matrix components of the BBB. Using a Boyden chamber assay system as an in vitro model of lymphocyte migration, we could show an increased rate of migration of lymphocytes derived from MS patients compared to controls, through a barrier comprised either of fibronectin alone or of endothelial cells (EC) derived from adult human CNS microvessels. Migration could be partially inhibited by matrix metalloproteinase (MMP) inhibitors and antibodies to MCP-1, the major lymphocyte chemoatractant produced by the ECs. Although the ECs can be induced to express both MHC class II and co-stimulatory molecules (B7-1), they favor induction of T cell anergy rather than proliferation. The perivascular microglia are the fully functional antigen presenting cells (APCs) at the level of the BBB. Parenchymal cell-lymphocyte interactions-within the human adult CNS, microglia can express both MHC class II and co-stimulatory molecules; in vitro studies indicate their capacity to process and present antigen. In contrast, adult human astrocytes can be induced to express only MHC class II molecules. They do not support classical antigen induced T cell proliferation but can support super-antigen induced responses. Parenchymal microglia are a source of the cytokine IL-12 that biases the T cell response toward a Th1 phenotype. In context of primary immune-mediated disease, the immune-glial cell network of interactive events is likely initiated by the former (e.g. via CD40-CD40L signaling). In context of neurodegenerative or chronic inflammatory CNS disorders, neural cells may play the central role in initiating or sustaining the response." @default.
• W1520697345 created "2016-06-24" @default.
• W1520697345 creator A5074910128 @default.
• W1520697345 date "2001-01-01" @default.
• W1520697345 modified "2023-09-25" @default.
• W1520697345 title "Regulation of the immune response within the central nervous system" @default.
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• W1520697345 doi "https://doi.org/10.1016/s1567-7443(01)80010-7" @default.
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