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Pathology studies of progressive multiple sclerosis (MS) indicate a major role of inflammation including Th17-cells and meningeal inflammation with ectopic lymphoid follicles, B-cells and plasma cells, the latter indicating a possible role of the newly identified subset of follicular T-helper (TFH) cells. Although previous studies reported increased(More)
OBJECTIVE Natalizumab inhibits the migration of systemic immune cells to the CNS and may be beneficial in progressive multiple sclerosis (MS). The objective of the study was to examine the effects of natalizumab in progressive MS. METHODS In an open-label phase 2A study, 24 patients with progressive MS were included to receive natalizumab treatment for 60(More)
Autoreactive CD4+ T-cells are considered to play a major role in the pathogenesis of multiple sclerosis. In experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, exogenous and endogenous type I interferons restrict disease severity. Recombinant interferon-β is used for treatment of multiple sclerosis, and some untreated multiple(More)
In multiple sclerosis (MS), treatment with the monoclonal antibody natalizumab effectively reduces the formation of acute lesions in the central nervous system (CNS). Natalizumab binds the integrin very late antigen (VLA)-4, expressed on the surface of immune cells, and inhibits VLA-4 dependent transmigration of circulating immune-cells across the vascular(More)
OBJECTIVE To investigate the effect of monthly oral methylprednisolone pulse treatment in progressive MS. METHODS 30 progressive MS patients were treated with oral methylprednisolone every month. Peripheral blood mononuclear cells were analyzed by flow cytometry. RESULTS Out of 102 leukocyte phenotypes investigated, 25 changed at nominal significance(More)
OBJECTIVE We aimed to investigate the role of oxidative stress in the progression of multiple sclerosis (MS). METHODS We determined by liquid chromatography-tandem mass spectrometry nonenzymatic (F2-isoprostanes) and enzymatic oxidation products of arachidonic acid (prostaglandin F2α [PGF2α]) in plasma and CSF of 45 controls (other neurologic disease(More)
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