TY  - JOUR
AU  - Stojanović, Ivana D.
AU  - Saksida, Tamara
AU  - Lazaroski, Sandra
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1478
AB  - 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.
PB  - Hoboken: John Wiley and Sons
T2  - Immunology
T1  - Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells
IS  - 1
VL  - 126
DO  - 10.1111/j.1365-2567.2008.02879.x
SP  - 74
EP  - 83
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1478
ER  - 

@article{
author = "Stojanović, Ivana D. and Saksida, Tamara and Lazaroski, Sandra and Stošić-Grujičić, Stanislava and Miljković, Đorđe",
year = "2009",
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.",
publisher = "Hoboken: John Wiley and Sons",
journal = "Immunology",
title = "Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells",
number = "1",
volume = "126",
doi = "10.1111/j.1365-2567.2008.02879.x",
pages = "74-83",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1478"
}

Stojanović, I. D., Saksida, T., Lazaroski, S., Stošić-Grujičić, S.,& Miljković, Đ.. (2009). Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells. in Immunology
Hoboken: John Wiley and Sons., 126(1), 74-83.
https://doi.org/10.1111/j.1365-2567.2008.02879.x
https://hdl.handle.net/21.15107/rcub_ibiss_1478

Stojanović ID, Saksida T, Lazaroski S, Stošić-Grujičić S, Miljković Đ. Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells. in Immunology. 2009;126(1):74-83.
doi:10.1111/j.1365-2567.2008.02879.x
https://hdl.handle.net/21.15107/rcub_ibiss_1478 .

Stojanović, Ivana D., Saksida, Tamara, Lazaroski, Sandra, Stošić-Grujičić, Stanislava, Miljković, Đorđe, "Macrophage migration inhibitory factor stimulates interleukin-17 expression and production in lymph node cells" in Immunology, 126, no. 1 (2009):74-83,
https://doi.org/10.1111/j.1365-2567.2008.02879.x .,
https://hdl.handle.net/21.15107/rcub_ibiss_1478 .