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      A Systematic Review of Several Potential Non-Genetic Risk Factors for Multiple Sclerosis

      ,

      Neuroepidemiology

      S. Karger AG

      Multiple sclerosis, Review, Sunlight, Sex hormones, Dietary fats

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          Abstract

          We reviewed the literature published in the English language to determine the weight of evidence for several potential non-genetic risk factors for multiple sclerosis, including solar ultraviolet radiation (UVR), sex hormones and dietary fat/fatty acids. We ranked the plausibility of each factor and graded the methodological rigour of case-control and cohort studies to determine whether there was a sufficient number of high-quality studies to weigh the evidence. Based on our criteria, the plausibility for solar UVR and sex hormones is good and fair for dietary fat/fatty acids. However, the body of epidemiologic evidence is insufficient for these three sets of risk factors. We did not find a sufficient number of methodologically rigorous studies to weigh the evidence for any of the potential risk factors we examined.

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          Most cited references 22

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          Vitamin D: its role and uses in immunology.

          In recent years there has been an effort to understand possible noncalcemic roles of vitamin D, including its role in the immune system and, in particular, on T cell-medicated immunity. Vitamin D receptor is found in significant concentrations in the T lymphocyte and macrophage populations. However, its highest concentration is in the immature immune cells of the thymus and the mature CD-8 T lymphocytes. The significant role of vitamin D compounds as selective immunosuppressants is illustrated by their ability to either prevent or markedly suppress animal models of autoimmune disease. Results show that 1,25-dihydroxyvitamin D3 can either prevent or markedly suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erythematosus, type I diabetes, and inflammatory bowel disease. In almost every case, the action of the vitamin D hormone requires that the animals be maintained on a normal or high calcium diet. Possible mechanisms of suppression of these autoimmune disorders by the vitamin D hormone have been presented. The vitamin D hormone stimulates transforming growth factor TGFbeta-1 and interleukin 4 (IL-4) production, which in turn may suppress inflammatory T cell activity. In support of this, the vitamin D hormone is unable to suppress a murine model of the human disease multiple sclerosis in IL-4-deficient mice. The results suggest an important role for vitamin D in autoimmune disorders and provide a fertile and interesting area of research that may yield important new therapies.
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            Effects of gender and sex steroids on the immune response.

            Elevated immune responses and the higher incidence of autoimmune diseases in female (compared to male) humans and animals have been known for a long time. However, the scientific interest in this interrelationship has been limited both amongst immunologists and endocrinologists. It is mainly in the last ten years that investigations in this area have been intensifying. A number of fairly recent review articles confirm the increased interest in various aspects of this "interdiscipline" [1-4]. In the present paper we should like to make a new assessment of the state of knowledge. We shall firstly discuss heteroimmune response differences between males and females in humans, rodents and birds and then the roles of gender and sex hormones in autoimmune disease in various species. The general conclusions are the following. Gender and sex hormones have a clear effect on various hetero- and auto-immune responses but the mechanisms of action are still unknown; starting from sex hormones, steroids can be devised which have favourable effects on immune processes but lack undesirable hormonal effects; such hormonomimetics should be, in principle, applicable for the treatment of autoimmune disease.
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              Prevention of experimental autoimmune encephalomyelitis by antibodies against interleukin 12

              Experimental allergic encephalomyelitis (EAE) is an autoimmune disease of the central nervous system that can be transferred to naive mice via CD4+ T cells isolated from appropriately immunized mice. We have evaluated the effects of recombinant murine interleukin 12 (rmIL-12), a potent inducer of interferon gamma (IFN-gamma) and promoter of Th1 T cell development, on the course of adoptively transferred EAE. The transfer of lymph node cells (LNC) isolated from proteolipid protein (PLP)-primed animals and stimulated in vitro with PLP to naive mice resulted in a progressive paralytic disease culminating in complete hind limb paralysis in the majority of the recipients. When mice were injected with LNC that had been stimulated in vitro with PLP in the presence of rmIL-12, the subsequent course of disease was more severe and prolonged. The addition of rmIL-12 during the in vitro stimulation with PLP resulted in a 10-fold increase in IFN-gamma and a 2-fold increase in tumor necrosis factor (TNF) alpha in the supernatants, relative to LNC stimulated with PLP alone. However, neutralization of IFN-gamma or TNF-alpha in vitro with specific antibodies did not abrogate the ability of rmIL-12 to exacerbate the subsequent disease. Similarly, mice treated with rmIL-12 in vivo after the transfer of antigen-stimulated LNC developed a more severe and prolonged course of disease compared with vehicle-treated control animals. In contrast, treatment of mice with an antibody to murine IL-12 after cell transfer completely prevented paralysis, with only 40% of the mice developing mild disease. These results demonstrate that in vitro stimulation of antigen primed LNC with PLP and rmIL-12 enhances their subsequent encephalitogenicity. Furthermore, inhibition of endogenous IL-12 in vivo after LNC transfer prevented paralysis, suggesting that endogenous IL-12 plays a pivotal role in the pathogenesis of this model of autoimmune disease.
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                Author and article information

                Journal
                NED
                Neuroepidemiology
                10.1159/issn.0251-5350
                Neuroepidemiology
                S. Karger AG
                0251-5350
                1423-0208
                2004
                April 2004
                23 January 2004
                : 23
                : 1-2
                : 1-12
                Affiliations
                Department of Community Health and Epidemiology, Queen’s University, Kingston, Ont., Canada
                Article
                73969 Neuroepidemiology 2004;23:1–12
                10.1159/000073969
                14739563
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 4, References: 103, Pages: 12
                Categories
                Review Paper

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