dc.creator | Stojanović, Ivana D. | |
dc.creator | Saksida, Tamara | |
dc.creator | Lazaroski, Sandra | |
dc.creator | Stošić-Grujičić, Stanislava | |
dc.creator | Miljković, Đorđe | |
dc.date.accessioned | 2017-11-23T11:12:38Z | |
dc.date.available | 2900-01-01 | |
dc.date.issued | 2009 | sr |
dc.identifier.issn | 0019-2805 | sr |
dc.identifier.other | Rad_konverzija_3473 | sr |
dc.identifier.uri | https://radar.ibiss.bg.ac.rs/handle/123456789/1478 | |
dc.description.abstract | Interleukin (IL)-17 is a pro-inflammatory cytokine produced by recently described T helper type 17 (Th17) cells, which have critical role in immunity to extracellular bacteria and the pathogenesis of several autoimmune disorders. IL-6 and transforming growth factor (TGF)-beta are crucial for the generation of Th17 cells in mice, while the production of IL-17 is supported by various cytokines, including IL-23, IL-1 beta, IL-21, IL-15 and tumour necrosis factor (TNF)-alpha. In this study, the influence of a multifunctional cytokine, macrophage migration inhibitory factor (MIF), on IL-17 production in mice was investigated. Treatment of lymph node cells (LNCs) with recombinant MIF up-regulated mitogen-stimulated IL-17 expression and secretion. Additionally, LNCs from MIF knockout mice (mif(-/-)) had severely impaired production of IL-17, as well as of IL-1 beta, IL-6, IL-23 and TGF-beta. When stimulated with recombinant IL-1 beta, IL-23 or TNF-alpha, mitogen-triggered mif(-/-) LNCs were fully able to achieve the IL-17 production seen in wild-type (WT) LNCs, while the addition of IL-6 and TGF-beta had no effect. Finally, after injection of mice with complete Freund's adjuvant, secretion of IL-17 as well as the number of IL-17-positive cells was significantly lower in the draining lymph nodes of mif(-/-) mice in comparison with WT mice. The effect of MIF on IL-17 production was dependent on p38, extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK) and Janus kinase 2/signal transducer and activator of transcription 3 (Jak2/STAT3), and not on nuclear factor (NF)-kappa B and nuclear factor of activated T cells (NFAT) signalling. Bearing in mind the contribution of MIF and IL-17 to the pathology of inflammatory and autoimmune disorders, from the results presented here it seems plausible that targeting MIF biological activity could be a valid therapeutic approach for the treatment of such diseases. | en |
dc.description.sponsorship | Serbian Ministry of Science [143029B] | sr |
dc.language.iso | English | sr |
dc.publisher | Hoboken: John Wiley and Sons | |
dc.relation | info:eu-repo/grantAgreement/MESTD/MPN2006-2010/143029/RS// | |
dc.rights | restrictedAccess | |
dc.source | Immunology | sr |
dc.title | Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells | en |
dc.type | article | |
dc.rights.license | ARR | |
dcterms.abstract | Стошић-Грујичић, Станислава Д.; Стојановић, Ивана Т; Цвјетичанин, Тамара; Лазароски, Сандра; Миљковић, Ђорђе М.; | |
dc.rights.holder | © 2008 The Authors Journal compilation © 2008 Blackwell Publishing Ltd | |
dc.citation.issue | 1 | sr |
dc.citation.volume | 126 | sr |
dc.identifier.doi | 10.1111/j.1365-2567.2008.02879.x | |
dc.identifier.pmid | 18624729 | |
dc.identifier.scopus | 2-s2.0-57449119699 | |
dc.identifier.wos | 000261528300009 | |
dc.citation.spage | 74 | |
dc.citation.epage | 83 | sr |
dc.type.version | publishedVersion | en |
dc.citation.rank | M22 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_1478 | |