Neurology

Neurology. of the interplay between T cells and B cells in MS may permit the development of B cell centered therapies that do not require depletion of this important cell populace. 1. MS AND RELATED INFLAMMATORY DEMYELINATING CNS DISEASES Multiple sclerosis (MS) is the most common neurological disease in young adults, influencing over 250,000 individuals in the United States and up to 1 1.2 million worldwide. It is believed to result from an autoimmune assault on protein components of myelin, the insulation which allows for quick conductance of electrical signals along axons. MS is definitely characterized by discrete regions of central nervous system (CNS) swelling, lymphocyte infiltration, demyelination, axonal damage, and ultimately the death of myelin-producing oligodendrocytes. Depending on the localization of these plaques, MS individuals suffer from a wide variety of symptoms, including weakness, sensory Gimeracil disturbances, ataxia, and visual impairment. Magnetic resonance imaging (MRI) allows visualization of active lesions in the absence of medical symptoms, and has become a useful tool for both analysis and monitoring of disease activity. A analysis of MS requires multiple episodes of demyelination separated in space and time (Poser and studies with purified or recombinant antibodies will become necessary to distinguish between these options. Now that medical tests with Rituximab have verified Gimeracil that B cells play an important part in the pathogenesis of MS, more selective methods can be tested that target either defined B cell populations or functions. Because plasma cells are maintained and autoantibody titers do not decrease in all individuals following B cell depletion, the beneficial effects of Rituximab in MS suggest that additional B cell functions are critical, such as antigen demonstration to T cells having a coordinating antigen specificity and/or cytokine and chemokine production. Rather than depleting B cells systemically, it may be preferable to decrease levels of prosurvival factors for which autoreactive cells must compete or block the cytokines required for perpetuation of an autoimmune response. A soluble version of the BAFF receptor offers successfully been used to treat and prevent MOG-induced EAE (Huntington delivery of small interfering RNAs via cell-surface receptors. Nat. Biotechnol. 2005;23(6):709C717. [PubMed] [Google Scholar]Sospedra M, Martin R. Immunology of multiple sclerosis. Annu. Rev. Immunol. 2005;23(1):683C747. [PubMed] [Google Scholar]Storch MK, Piddlesden S, Haltia M, Iivanainen M, Morgan P, Lassmann H. Multiple sclerosis: evidence for antibody- and complement-mediated demyelination. Ann. Neurol. 1998;43(4):465C471. [PubMed] [Google Scholar]Stromnes IM, Goverman JM. Active induction Gimeracil of experimental sensitive encephalomyelitis. Nat. Protoc. 2006a;1(4):1810C1819. [PubMed] [Google Scholar]Stromnes IM, Goverman JM. Passive induction of experimental allergic encephalomyelitis. Nat. Protoc. 2006b;1(4):1952C1960. [PubMed] [Google Scholar]Stuve O, Cepok S, Elias B, Saleh A, Hartung H-P, Hemmer B, Kieseier BC. Clinical stabilization and effective B-lymphocyte depletion in the cerebrospinal fluid Rabbit polyclonal to CAIX and peripheral blood of a patient with fulminant relapsing-remitting multiple sclerosis. Arch. Neurol. 2005;62(10):1620C1623. [PubMed] [Google Scholar]Svensson L, Abdul-Majid K-B, Bauer J, Lassmann H, Harris RA, Holmdahl R. A comparative analysis of B cell-mediated myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis pathogenesis in B cell-deficient mice discloses an effect on demyelination. Eur. J. Immunol. 2002;32(7):1939C1946. [PubMed] [Google Scholar]Takahashi T, Fujihara K, Nakashima I, Misu T, Miyazawa I, Nakamura M, Watanabe S, Shiga Y, Kanaoka C, Fujimori J, Sato S, Itoyama Y. Antiaquaporin-4 antibody is definitely involved in the pathogenesis of NMO: A study on antibody titre. Mind. 2007;130(5):1235C1243. [PubMed] [Google Scholar]Tanaka Y, Yamamoto K, Takeuchi T, Nishimoto N, Miyasaka N, Sumida Gimeracil T, Shima Y, Takada K, Matsumoto I, Saito K, Koike T. A multicenter phase I/II trial of rituximab for refractory systemic lupus erythematosus. Mod. Rheumatol. 2007;17(3):191C197. [PubMed] [Google Scholar]Tenembaum S, Chamoles N, Fejerman N. Acute disseminated encephalomyelitis: A long-term follow-up study of 84 pediatric individuals. Neurology. 2002;59(8):1224C1231. [PubMed] [Google Scholar]Tenembaum S, Chitnis T, Ness J,.