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dc.creatorPilipović, Ivan
dc.creatorStojić-Vukanić, Zorica
dc.creatorPrijić, Ivana
dc.creatorLeposavić, Gordana
dc.date.accessioned2021-02-18T10:54:14Z
dc.date.available2021-02-18T10:54:14Z
dc.date.issued2020
dc.identifier.issn1664-2392
dc.identifier.urihttp://intor.torlakinstitut.com/handle/123456789/571
dc.description.abstractThe role of stress effector systems in the initiation and progression of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the most commonly used experimental model of MS, has strongly been suggested. To corroborate this notion, alterations in activity of the sympathoadrenal and sympathoneural axes of sympathoadrenal system (a major communication pathway between the central nervous system and the immune system), mirrored in altered release of their end-point mediators (adrenaline and noradrenaline, respectively), are shown to precede (in MS) and/or occur during development of MS and EAE in response to immune cell activation (in early phase of disease) and disease-related damage of sympathoadrenal system neurons and their projections (in late phase of disease). To add to the complexity, innate immunity cells and T-lymphocytes synthesize noradrenaline that may be implicated in a local autocrine/paracrine self-amplifying feed-forward loop to enhance myeloid-cell synthesis of proinflammatory cytokines and inflammatory injury. Furthermore, experimental manipulations targeting noradrenaline/adrenaline action are shown to influence clinical outcome of EAE, in a disease phase-specific manner. This is partly related to the fact that virtually all types of cells involved in the instigation and progression of autoimmune inflammation and target tissue damage in EAE/MS express functional adrenoceptors. Although catecholamines exert majority of immunomodulatory effects through beta(2)-adrenoceptor, a role for alpha-adrenoceptors in EAE pathogenesis has also been indicated. In this review, we summarize all aforementioned aspects of immunopathogenetic action of catecholamines in EAE/MS as possibly important for designing new strategies targeting their action to prevent/mitigate autoimmune neuroinflammation and tissue damage.en
dc.publisherFrontiers Media Sa, Lausanne
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175050/RS//
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceFrontiers in Endocrinology
dc.subjectsympathoadrenal systemen
dc.subjectnoradrenalineen
dc.subjectbeta-adrenoceptoren
dc.subjectalpha-adrenoceptoren
dc.subjectexperimental autoimmune encephalomyelitisen
dc.subjectmultiple sclerosisen
dc.titleRole of the End-Point Mediators of Sympathoadrenal and Sympathoneural Stress Axes in the Pathogenesis of Experimental Autoimmune Encephalomyelitis and Multiple Sclerosisen
dc.typearticle
dc.rights.licenseBY
dc.citation.other10
dc.citation.rankM22~
dc.citation.volume10
dc.identifier.doi10.3389/fendo.2019.00921
dc.identifier.fulltexthttp://intor.torlakinstitut.com/bitstream/id/381/568.pdf
dc.identifier.pmid31993021
dc.identifier.rcubconv_467
dc.identifier.scopus2-s2.0-85078785545
dc.identifier.wos000509902700001
dc.type.versionpublishedVersion


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