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dc.contributor.authorGhalamfarsa, G
dc.contributor.authorMahmoudi, M
dc.contributor.authorMohammadnia-Afrouzi, M
dc.contributor.authorYazdani, Y
dc.contributor.authorAnvari, E
dc.contributor.authorHadinia, A
dc.contributor.authorGhanbari, A
dc.contributor.authorSetayesh, M
dc.contributor.authorYousefi, M
dc.contributor.authorJadidi-Niaragh, F
dc.date.accessioned2018-08-26T07:28:26Z
dc.date.available2018-08-26T07:28:26Z
dc.date.issued2016
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/46969
dc.description.abstractCytokines are considered important factors in the modulation of various immune responses. Among them, interleukin (IL)-21 is one of the major immune modulators, adjusting various immune responses by affecting various immune cells. It has been suggested that IL-21 may enhance autoimmunity through different mechanisms, such as development and activation of helper T (T-H)-17 and follicular helper T (T-FH) cells, activation of natural killer (NK) cells, enhancing B-cell differentiation and antibody secretion and suppression of regulatory T (T-reg) cells. Moreover, IL-21 has also been suggested to be an inducer of autoimmunity when following treatment of MS patients with some therapeutics such as alemtuzumab. This review will seek to clarify the precise role of IL-21/IL-21R in the pathogenesis of MS and, in its animal model, experimental autoimmune encephalomyelitis (EAE).
dc.language.isoEnglish
dc.relation.ispartofJOURNAL OF IMMUNOTOXICOLOGY
dc.subjectInterleukin (IL)-21
dc.subjectIL-21 receptor
dc.subjectmultiple sclerosis
dc.subjectpathogenesis
dc.titleIL-21 and IL-21 receptor in the immunopathogenesis of multiple sclerosis
dc.typeReview
dc.citation.volume13
dc.citation.issue3
dc.citation.spage274
dc.citation.epage285
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.3109/1547691X.2015.1089343


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