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      Update on immunopathogenesis and immunotherapy in multiple sclerosis

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          Abstract

          Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system. Both genetic and environmental factors are believed to contribute to the pathogenesis of the disease. Histopathological findings suggest that multiple sclerosis is an immune-mediated disease, involving both the cellular and humoral immune systems. Within the last 20 years, several disease-modifying therapies for the treatment of multiple sclerosis were established. Moreover, promising new substances are currently being tested in clinical trials and will likely broaden the therapeutic opportunities available within the upcoming years.

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          Naturally arising Foxp3-expressing CD25+CD4+ regulatory T cells in immunological tolerance to self and non-self.

          Shimon Sakaguchi (2005)
          Naturally arising CD25(+)CD4(+) regulatory T cells actively maintain immunological self-tolerance. Deficiency in or dysfunction of these cells can be a cause of autoimmune disease. A reduction in their number or function can also elicit tumor immunity, whereas their antigen-specific population expansion can establish transplantation tolerance. They are therefore a good target for designing ways to induce or abrogate immunological tolerance to self and non-self antigens.
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            Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial.

            Jeffrey A Cohen, Alasdair J Coles, Douglas L Arnold … (2012)
            The anti-CD52 monoclonal antibody alemtuzumab reduced disease activity in a phase 2 trial of previously untreated patients with relapsing-remitting multiple sclerosis. We aimed to assess efficacy and safety of first-line alemtuzumab compared with interferon beta 1a in a phase 3 trial. In our 2 year, rater-masked, randomised controlled phase 3 trial, we enrolled adults aged 18-50 years with previously untreated relapsing-remitting multiple sclerosis. Eligible participants were randomly allocated in a 2:1 ratio by an interactive voice response system, stratified by site, to receive intravenous alemtuzumab 12 mg per day or subcutaneous interferon beta 1a 44 μg. Interferon beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baseline and once per day for 3 days at 12 months. Coprimary endpoints were relapse rate and time to 6 month sustained accumulation of disability in all patients who received at least one dose of study drug. This study is registered with ClinicalTrials.gov, number NCT00530348. 187 (96%) of 195 patients randomly allocated interferon beta 1a and 376 (97%) of 386 patients randomly allocated alemtuzumab were included in the primary analyses. 75 (40%) patients in the interferon beta 1a group relapsed (122 events) compared with 82 (22%) patients in the alemtuzumab group (119 events; rate ratio 0·45 [95% CI 0·32-0·63]; p<0.0001), corresponding to a 54·9% improvement with alemtuzumab. Based on Kaplan-Meier estimates, 59% of patients in the interferon beta 1a group were relapse-free at 2 years compared with 78% of patients in the alemtuzumab group (p<0·0001). 20 (11%) of patients in the interferon beta 1a group had sustained accumulation of disability compared with 30 (8%) in the alemtuzumab group (hazard ratio 0·70 [95% CI 0·40-1·23]; p=0·22). 338 (90%) of patients in the alemtuzumab group had infusion-associated reactions; 12 (3%) of which were regarded as serious. Infections, predominantly of mild or moderate severity, occurred in 253 (67%) patients treated with alemtuzumab versus 85 (45%) patients treated with interferon beta 1a. 62 (16%) patients treated with alemtuzumab had herpes infections (predominantly cutaneous) compared with three (2%) patients treated with interferon beta 1a. By 24 months, 68 (18%) patients in the alemtuzumab group had thyroid-associated adverse events compared with 12 (6%) in the interferon beta 1a group, and three (1%) had immune thrombocytopenia compared with none in the interferon beta 1a group. Two patients in the alemtuzumab group developed thyroid papillary carcinoma. Alemtuzumab's consistent safety profile and benefit in terms of reductions of relapse support its use for patients with previously untreated relapsing-remitting multiple sclerosis; however, benefit in terms of disability endpoints noted in previous trials was not observed here. Genzyme (Sanofi) and Bayer Schering Pharma. Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Environmental risk factors for multiple sclerosis. Part I: the role of infection.

              Alberto Ascherio, Kassandra L Munger (2007)
              Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the "hygiene hypothesis," but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. The role of infectious factors is discussed here; in a companion article, we will examine the possible role of noninfectious factors and provide evidence that high levels of vitamin D may have a protective role, particularly during adolescence. The primary purpose of these reviews is to identify clues to the causes of MS and to evaluate the possibility of primary prevention.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Immunotargets Ther
                Journal ID (iso-abbrev): Immunotargets Ther
                Journal ID (publisher-id): ImmunoTargets and Therapy
                Title: ImmunoTargets and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 2253-1556
                Publication date Collection: 2013
                Publication date (Electronic): 25 April 2013
                Volume: 2
                Pages: 21-30
                Affiliations
                [1 ]Department of Neurology, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany
                [2 ]Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
                [3 ]Competence Network on Multiple Sklerosis, Munich, Germany
                Author notes
                Correspondence: Bernhard Hemmer, Department of Neurology, Klinikum Rechts der Isar, Technische Universität München, Ismaninger Strasse 22, Munich 81675, Germany, Tel +49 89 4140 4600, Fax +49 89 4140 7681, Email hemmer@ 123456lrz.tum.de
                Article
                Publisher ID: itt-2-021
                DOI: 10.2147/ITT.S31813
                PMC ID: 4928362
                PubMed ID: 27471685
                SO-VID: 319aa6ab-ab44-4bb2-89a9-29d9873dc705
                Copyright © © 2013 Selter and Hemmer, publisher and licensee Dove Medical Press Ltd
                License:

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                Categories
                Subject: Review

                Keywords: multiple sclerosis,immunopathogenesis,disease-modifying therapy
                Data availability:
                Keywords: multiple sclerosis, immunopathogenesis, disease-modifying therapy

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