[Blood-brain barrier in multiple sclerosis: mechanisms of its breakdown and repair].
The blood-brain barrier(BBB) restricts exchanges of soluble factors and cells between the blood and brain, thus playing a crucial role in maintenance of cerebral homeostasis. In multiple sclerosis(MS), disruption of the BBB is the initial key step in the development of inflammatory lesions. BBB impairment may occur before the formation of demyelinative foci or T cell infiltration around small vessels; however, once the BBB breaks, massive infiltration of T cells, augmented expression of adhesion molecules on endothelial cell surface, and leakage of inflammatory cytokines and antibodies will aggravate the MS lesions. Although glucocorticoids and type 1 interferons are now widely used and are known to decrease BBB permeability additively, the development of novel therapeutic strategy focusing on the repairment of BBB integrity should be awaited.
Kanda
Takashi
T
Department of Neurology and Neurological Science, Tokyo Medical and Dental University Graduate School.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D001812:Blood-Brain Barrier / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004359:Drug Therapy, Combination; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D000068717:Glatiramer Acetate; D006801:Humans; D016899:Interferon-beta / Q000627:therapeutic use; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000209:etiology*; D010455:Peptides / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000276:immunology
D000305:Adrenal Cortex Hormones; D015815:Cell Adhesion Molecules; D016207:Cytokines; D010455:Peptides; D000068717:Glatiramer Acetate; D016899:Interferon-beta