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- Title
EXISTING IMMUNOMODULATORY THERAPY AND POTENTIAL NEUROPROTECTIVE ROLES.
- Authors
Stüve, Olaf
- Abstract
Six disease-modifying therapies are approved for the treatment of multiple sclerosis: glatiramer acetate, 2 formulations of interferon (IFN) β-1α (one administered by subcutaneous injection and one administered by intramuscular injection), IFNβ-1b, natalizumab, and mitoxantrone. These agents are thought to act primarily by suppressing central nervous system (CNS) inflammation, which may also produce secondary neuroprotective effects. Inflammatory CNS demyelination requires a sequence of tightly controlled immune processes, including antigen presentation to T cells, additional cell-cell contacts between antigen-presenting cells and T cells that are required for full T-cell activation, the migration of T cells through the endothelial lining, and the release of several proinflammatory or anti-inflammatory chemical mediators. IFNβ and glatiramer acetate (GA) interrupt several of these process, resulting in decreased CNS infiltration of lymphocytes and inflammation. GA may also produce neuroprotective effects by modulating the release of neurotrophic factors, chemical mediators that are produced by several cell populations that promote neuronal development and survival. Natalizumab blocks specific cell-surface receptor molecules that are required for lymphocytes to migrate from the circulation to the CNS, producing long-lasting suppression of the infiltration of CD4+ and CD8+ T lymphocytes. Natalizumab may produce a rebound increase in the number of T2 lesions on magnetic resonance imaging after discontinuation. Mitoxantrone is an antineoplastic agent that interferes with DNA replication in rapidly dividing cells, resulting in lymphocyte depletion. It is not known to produce neuroprotective effects.
- Publication
Johns Hopkins Advanced Studies in Medicine, 2008, Vol 8, Issue 9, p315
- ISSN
1530-3004
- Publication type
Academic Journal