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dc.contributor.authorSafarzadeh, E
dc.contributor.authorJadidi-Niaragh, F
dc.contributor.authorMotallebnezhad, M
dc.contributor.authorYousefi, M
dc.date.accessioned2018-08-26T07:27:21Z
dc.date.available2018-08-26T07:27:21Z
dc.date.issued2016
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/46868
dc.description.abstractIntroduction Multiple sclerosis (MS) is a heterogeneous neurological disorder with multifactorial etiologies characterized by demyelination, axonal degeneration, and oligodendroglial death. It is believed that both genetics and environmental risk factors such as infection are involved in disease etiology. Accumulating evidence indicates that alteration in purinergic system signaling is involved in immunity and inflammation. Adenosine, a key purine nucleoside, has been shown to be produced during metabolic stress, including ischemia, inflammatory condition, and tissue injury. Methods Extracellular adenosine directly affects various physiological and pathological processes of MS by stimulating G protein-coupled adenosine receptors A1, A2A, A2B, and A3 on the surface of immune cells. It has been suggested that promotion of adenosinergic system may be an important factor in MS pathophysiology and considered as promising therapeutic target for this disease. Conclusion In this review, we will discuss about the immunopathologic effects of adenosine on MS and its animal model, experimental autoimmune encephalomyelitis.
dc.language.isoEnglish
dc.relation.ispartofINFLAMMATION RESEARCH
dc.subjectAdenosine
dc.subjectAdenosine receptor
dc.subjectMultiple sclerosis
dc.subjectExperimental autoimmune encephalomyelitis
dc.titleThe role of adenosine and adenosine receptors in the immunopathogenesis of multiple sclerosis
dc.typeReview
dc.citation.volume65
dc.citation.issue7
dc.citation.spage511
dc.citation.epage520
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1007/s00011-016-0936-z


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