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      Hormones in experimental autoimmune encephalomyelitis (EAE) animal models

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          Abstract

          Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) in which activated immune cells attack the CNS and cause inflammation and demyelination. While the etiology of MS is still largely unknown, the interaction between hormones and the immune system plays a role in disease progression, but the mechanisms by which this occurs are incompletely understood. Several in vitro and in vivo experimental, but also clinical studies, have addressed the possible role of the endocrine system in susceptibility and severity of autoimmune diseases. Although there are several demyelinating models, experimental autoimmune encephalomyelitis (EAE) is the oldest and most commonly used model for MS in laboratory animals which enables researchers to translate their findings from EAE into human. Evidences imply that there is great heterogeneity in the susceptibility to the induction, the method of induction, and the response to various immunological or pharmacological interventions, which led to conflicting results on the role of specific hormones in the EAE model. In this review, we address the role of endocrine system in EAE model to provide a comprehensive view and a better understanding of the interactions between the endocrine and the immune systems in various models of EAE, to open up a ground for further detailed studies in this field by considering and comparing the results and models used in previous studies.

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          Most cited references190

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          Multiple Sclerosis

          New England Journal of Medicine, 343(13), 938-952
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            Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS).

            Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the human inflammatory demyelinating disease, multiple sclerosis (MS). EAE is a complex condition in which the interaction between a variety of immunopathological and neuropathological mechanisms leads to an approximation of the key pathological features of MS: inflammation, demyelination, axonal loss and gliosis. The counter-regulatory mechanisms of resolution of inflammation and remyelination also occur in EAE, which, therefore can also serve as a model for these processes. Moreover, EAE is often used as a model of cell-mediated organ-specific autoimmune conditions in general. EAE has a complex neuropharmacology, and many of the drugs that are in current or imminent use in MS have been developed, tested or validated on the basis of EAE studies. There is great heterogeneity in the susceptibility to the induction, the method of induction and the response to various immunological or neuropharmacological interventions, many of which are reviewed here. This makes EAE a very versatile system to use in translational neuro- and immunopharmacology, but the model needs to be tailored to the scientific question being asked. While creating difficulties and underscoring the inherent weaknesses of this model of MS in straightforward translation from EAE to the human disease, this variability also creates an opportunity to explore multiple facets of the immune and neural mechanisms of immune-mediated neuroinflammation and demyelination as well as intrinsic protective mechanisms. This allows the eventual development and preclinical testing of a wide range of potential therapeutic interventions. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
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              RAMPs regulate the transport and ligand specificity of the calcitonin-receptor-like receptor.

              Calcitonin-gene-related peptide (CGRP) and adrenomedullin are related peptides with distinct pharmacological profiles. Here we show that a receptor with seven transmembrane domains, the calcitonin-receptor-like receptor (CRLR), can function as either a CGRP receptor or an adrenomedullin receptor, depending on which members of a new family of single-transmembrane-domain proteins, which we have called receptor-activity-modifying proteins or RAMPs, are expressed. RAMPs are required to transport CRLR to the plasma membrane. RAMP1 presents the receptor at the cell surface as a mature glycoprotein and a CGRP receptor. RAMP2-transported receptors are core-glycosylated and are adrenomedullin receptors.
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                Author and article information

                Contributors
                Journal
                Transl Neurosci
                Transl Neurosci
                tnsci
                Translational Neuroscience
                De Gruyter
                2081-3856
                2081-6936
                06 May 2021
                01 January 2021
                : 12
                : 1
                : 164-189
                Affiliations
                Neuroscience Laboratory, CHU de Québec Research Center and Department of Molecular Medicine, Faculty of Medicine, Laval University , Québec City, QC, Canada
                Cellular and Molecular Research Center, Yasuj University of Medical Sciences , Yasuj, Iran
                Biomedical and Pharmaceutical Research Unit and Department of Basic Medical Sciences, College of Medicine , QU Health, Qatar University, Doha, Qatar
                Department of Biological and Chemical Sciences, Faculty of Arts and Sciences, Lebanese International University , Beirut, Lebanon
                Clinical Pharmacology Department, Menoufia Medical School, Menoufia University , Shibin Al Kawm, Egypt
                Department of Basic Medical Sciences, Kulliyyah of Medicine, International Islamic University Malaysia (IIUM) , Kuantan, Pahang, Malaysia
                Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina , Messina, Italy
                PRASE, Lebanese University , Beirut, Lebanon
                Biology Department, Faculty of Sciences – I, Lebanese University , Beirut, Lebanon
                Article
                tnsci-2020-0169
                10.1515/tnsci-2020-0169
                8134801
                34046214
                06aefe9c-78f9-47bd-9ca5-7ffdd37dcbba
                © 2021 Majid Ghareghani et al., published by De Gruyter

                This work is licensed under the Creative Commons Attribution 4.0 International License.

                History
                : 17 January 2021
                : 05 April 2021
                : 14 April 2021
                Page count
                Pages: 26
                Categories
                Review Article

                multiple sclerosis,experimental autoimmune encephalomyelitis,eae,endocrine system,hormone

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