title: [Pathogenesis and therapy of multiple sclerosis].
abstract: Multiple sclerosis (MS) is one of the most frequent serious neurologic diseases. Etiologically, MS involves genetic, viral and other factors. The key pathogenic mechanisms reside in the autoimmune reaction of activated CD4+ T lymphocytes crossing the haematoencephalic barrier and attacking different epitopes of the basic protein and proteolipid of myelin sheaths. The damaging reaction involving activated macrophages, destructive inflammatory cytokines and toxic radicals leads to the development of disseminated plaques. The passage of autoimmune T lymphocytes to the brain tissue is facilitated by overexpression of adhesion molecules on endothelial cells, neural cells and immunocytes. The diagnosis of MS is based on characteristic changes in the blood and liquor, and on the results of modern methods, especially (gadolinium enhanced) MRI. The "classical" treatment is based on glucorticosteroids, azathioprine, cyclophosphamide and other chemicals which are not fully satisfactory and are accompanied by serious side-effects. Therefore, attention will be paid to three prospective biological methods of treatment: 1) peroral application of bovine myelin, its fractions, and synthetic copolymer-1, aimed at the restoration of immune tolerance; 2) injections of natural and recombinant interferon-beta, interfering with the pathogenic IFN-gamma and other cytokines; 3) systemic enzyme therapy (residing in peroral application of combinations of animal and herbal hydrolytic enzymes), which modulates adhesion molecules and suppresses the activation of autoimmune T lymphocytes. The chief results of clinical studies with respect to the effectiveness and safety of these therapeutic methods, will be summarized. (Ref. 34.)
authors.affiliation: Ustav pro péci o matku a ditĕ v Praze.
authors.forename: K
authors.initials: K
authors.lastname: Nouza
authors.forename: H
authors.initials: H
authors.lastname: Krejcová
mesh_terms: D006801:Humans; D009103:Multiple Sclerosis / Q000503:physiopathology / Q000628:therapy*