Monoclonal antibody treatments for multiple sclerosis.
Monoclonal antibodies (MAbs) may have great potential as therapies for autoimmune diseases. Their development as treatments for multiple sclerosis (MS) is promising. Partially effective immunomodulatory therapies have been helpful for many MS patients; however, for patients failing these immunomodulatory treatments, MAbs are an important new treatment option. Currently, MAbs are approved by the US Food and Drug Administration for treatment of many conditions, including autoimmune diseases. Four MAbs that have been investigated as potential treatments for MS are reviewed in this article. Of these MAbs, natalizumab is approved for treatment of MS. The other three MAbs (alemtuzumab, rituximab, and daclizumab) are all promising therapies in development for treatment of MS. Adverse effects are relatively mild for these MAbs; however, care in administration and management of these agents is emphasized. Overall, these MAb therapies have great promise in the treatment of MS.
Rose
John W
JW
Neurovirology Research Laboratory, VA Salt Lake City Health Care System; Department of Neurology, University of Utah Neurovirology Research Laboratory, Salt Lake City, UT 84148, USA. jrose@genetics.utah.edu
Foley
John
J
Carlson
Noel
N
D000074323:Alemtuzumab; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use; D000918:Antibody Specificity; D015703:Antigens, CD / Q000276:immunology; D018951:Antigens, CD20 / Q000276:immunology; D000951:Antigens, Neoplasm / Q000276:immunology; D001327:Autoimmune Diseases / Q000139:chemically induced; D000074301:CD52 Antigen; D002986:Clinical Trials as Topic / Q000706:statistics & numerical data; D003131:Combined Modality Therapy; D000077561:Daclizumab; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000276:immunology / Q000627:therapeutic use; D039441:Integrin alpha4 / Q000276:immunology; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology; D007968:Leukoencephalopathy, Progressive Multifocal / Q000139:chemically induced; D008206:Lymphatic Diseases / Q000139:chemically induced; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000276:immunology / Q000628:therapy*; D000069442:Natalizumab; D000069283:Rituximab; D012713:Serum Sickness / Q000139:chemically induced; D013921:Thrombocytopenia / Q000139:chemically induced
D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm; D015703:Antigens, CD; D018951:Antigens, CD20; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D007074:Immunoglobulin G; D053645:Interleukin-2 Receptor alpha Subunit; D000069442:Natalizumab; D039441:Integrin alpha4; D000074323:Alemtuzumab; D000069283:Rituximab; D000077561:Daclizumab