[Progress in unravelling the etiology of multiple sclerosis].
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Fortunately, progress has been made for patients with this devastating disorder thanks to the induction of novel treatment strategies. In the 1990s, autoimmunity against myelin-related proteins was verified in humans, while the molecular mechanisms of the pathological process resulting in CNS demyelination were also studied in depth using experimental autoimmune encephalomyelitis (EAE). In the present decade, those achievements led to clinical trials of a variety of monoclonal antibody reagents for preventing disease relapse. Although such treatment seems to be ideal, as it targets a specific harmful immune reaction on the basis of findings from EAE studies, it has yet to become a first-line strategy, because of, in part, unexpected serious adverse reactions. As a result, interferon-beta therapy, the efficacy of which was first reported in 1993. has maintained a good position among treatment options for suppressing disease activity. Interferon-beta is considered to exert its anti-inflammatory effect via a Th2 shift in immune responses. In addition to aberrant cellular immunity, recent progress in MS research has shed light on the involvement of disturbances in humoral immunity, including the presence of NMO-IgG and anti-aquaporin-4 antibodies. Thus, it is important to elucidate the pathological significance of those autoantibodies, as well as establish treatment strategies for patients who are positive for them. However, since the above-mentioned treatments have been developed only for patients with relapsing-remitting MS. it is also important to consider the pathogenesis of primary progressive MS, which constitutes 10-15% of the patient population. Neurologists cannot be indifferent to current studies on MS, as even viral etiologies long ago abandoned have been recently revisited. In this field of neurology, every step of progress may readily lead to the establishment of a new treatment options.
Matsui
Makoto
M
Department of Neurology, Kanazawa Medical University.
D000074323:Alemtuzumab; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm / Q000627:therapeutic use; D001323:Autoantibodies; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental; D006801:Humans; D016899:Interferon-beta / Q000627:therapeutic use; D008279:Magnetic Resonance Imaging; D009103:Multiple Sclerosis / Q000175:diagnosis / Q000209:etiology* / Q000276:immunology / Q000628:therapy; D009185:Myelin Proteins / Q000276:immunology; D000069283:Rituximab; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm; D001323:Autoantibodies; D009185:Myelin Proteins; D000074323:Alemtuzumab; D000069283:Rituximab; D016899:Interferon-beta