Glatiramer acetate Copaxone regulates nitric oxide and related cytokine secretion in experimental autoimmune encephalomyelitis

dc.authorid41809en_US
dc.contributor.authorKayhan, Başak
dc.contributor.authorAharoni, Rina
dc.contributor.authorArnon, Ruth
dc.date.accessioned2017-08-04T10:59:18Z
dc.date.available2017-08-04T10:59:18Z
dc.date.issued2003
dc.departmentİnönü Üniversitesien_US
dc.description.abstractNitric oxide (NO) is an important mediator involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS). We examined the effect of glatiramer acetate (GA), an agent with suppressing effect on EAE and of therapeutic value for the treatment of MS, on the secretion of NO, as well as of the NO regulating cytokines. We observed that induction of EAE leads to 4-fold elevation in NO secretion and that treatment of the EAE mice by GA indeed leads to a significant reduction in the NO secretion by the splenocytes in response to the encephalitogen. A parallel decrease was observed in the secretion of the NO inducing cytokine IL-1b. On the other hand, the secretion level of NO modulating cytokines IL-10 and IL-13 was significantly augmented. The correlation between these findings and the therapeutic effect of GA is discussed.en_US
dc.identifier.citationKayhan, B. Aharoni, R. Arnon, R. (2003). Glatiramer acetate Copaxone regulates nitric oxide and related cytokine secretion in experimental autoimmune encephalomyelitis. Immunology Lettersen_US
dc.identifier.doi10.1016/S0165-2478(03)00085-3en_US
dc.identifier.issn01652478
dc.identifier.urihttps://hdl.handle.net/11616/7445
dc.language.isoenen_US
dc.publisherImmunology Lettersen_US
dc.relation.ispartofImmunology Lettersen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectExperimental autoimmune encephalomyelitis (EAE)en_US
dc.subjectNitric oxide (NO)en_US
dc.subjectTh2 cytokinesen_US
dc.subjectCopaxoneen_US
dc.subjectGlatiramer acetate (GA)en_US
dc.titleGlatiramer acetate Copaxone regulates nitric oxide and related cytokine secretion in experimental autoimmune encephalomyelitisen_US
dc.typeArticleen_US

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