TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
AU  - Maksimović-Ivanić, Danijela
AU  - Momčilović, Miljana
AU  - Popadić, Dušan
AU  - Harhaji-Trajković, Ljubica
AU  - Miljković, Đorđe
AU  - Metz, Christine
AU  - Mangano, Katia
AU  - Papaccio, Gianpacilo
AU  - Al-Abed, Yousef
AU  - Nicoletti, Ferdinando
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1528
AB  - Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine of the innate immune system that plays a major role in the induction of immunoinflammatory responses. To examine the role of endogenous MIF in the pathogenesis of type I diabetes (TID) we evaluated the effects of administration of neutralizing anti-MIF antibodies to NOD mice with accelerated forms of diabetes induced by injection of cyclophosphamide or by transfer of diabetogenic spleen cells. Both accelerated forms of diabetes were markedly reduced by anti-MIF antibody. Furthermore, MIF-deficient (MIF(-/-)) mice were less susceptible to the induction of immunoinflammatory diabetes, insulitis and apoptosis within the endocrine pancreas by multiple low doses of streptozotocin (MLD-STZ) than genetically matched wild type (WT) mice. MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1 beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1 beta, and iNOS in the islets of Langerhans. These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-1-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. These results suggest that MIF participates in T1D by controlling the functional activity of monocytes/macrophages and T cells and modulating their secretory capacity of pro- and anti-inflammatory molecules.
PB  - John Wiley and Sons
T2  - Journal of Cellular Physiology
T1  - Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus
IS  - 3
VL  - 215
DO  - 10.1002/jcp.21346
SP  - 665
EP  - 675
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1528
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Stojanović, Ivana D. and Maksimović-Ivanić, Danijela and Momčilović, Miljana and Popadić, Dušan and Harhaji-Trajković, Ljubica and Miljković, Đorđe and Metz, Christine and Mangano, Katia and Papaccio, Gianpacilo and Al-Abed, Yousef and Nicoletti, Ferdinando",
year = "2008",
abstract = "Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine of the innate immune system that plays a major role in the induction of immunoinflammatory responses. To examine the role of endogenous MIF in the pathogenesis of type I diabetes (TID) we evaluated the effects of administration of neutralizing anti-MIF antibodies to NOD mice with accelerated forms of diabetes induced by injection of cyclophosphamide or by transfer of diabetogenic spleen cells. Both accelerated forms of diabetes were markedly reduced by anti-MIF antibody. Furthermore, MIF-deficient (MIF(-/-)) mice were less susceptible to the induction of immunoinflammatory diabetes, insulitis and apoptosis within the endocrine pancreas by multiple low doses of streptozotocin (MLD-STZ) than genetically matched wild type (WT) mice. MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1 beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1 beta, and iNOS in the islets of Langerhans. These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-1-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. These results suggest that MIF participates in T1D by controlling the functional activity of monocytes/macrophages and T cells and modulating their secretory capacity of pro- and anti-inflammatory molecules.",
publisher = "John Wiley and Sons",
journal = "Journal of Cellular Physiology",
title = "Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus",
number = "3",
volume = "215",
doi = "10.1002/jcp.21346",
pages = "665-675",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1528"
}

Stošić-Grujičić, S., Stojanović, I. D., Maksimović-Ivanić, D., Momčilović, M., Popadić, D., Harhaji-Trajković, L., Miljković, Đ., Metz, C., Mangano, K., Papaccio, G., Al-Abed, Y.,& Nicoletti, F.. (2008). Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. in Journal of Cellular Physiology
John Wiley and Sons., 215(3), 665-675.
https://doi.org/10.1002/jcp.21346
https://hdl.handle.net/21.15107/rcub_ibiss_1528

Stošić-Grujičić S, Stojanović ID, Maksimović-Ivanić D, Momčilović M, Popadić D, Harhaji-Trajković L, Miljković Đ, Metz C, Mangano K, Papaccio G, Al-Abed Y, Nicoletti F. Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. in Journal of Cellular Physiology. 2008;215(3):665-675.
doi:10.1002/jcp.21346
https://hdl.handle.net/21.15107/rcub_ibiss_1528 .

Stošić-Grujičić, Stanislava, Stojanović, Ivana D., Maksimović-Ivanić, Danijela, Momčilović, Miljana, Popadić, Dušan, Harhaji-Trajković, Ljubica, Miljković, Đorđe, Metz, Christine, Mangano, Katia, Papaccio, Gianpacilo, Al-Abed, Yousef, Nicoletti, Ferdinando, "Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus" in Journal of Cellular Physiology, 215, no. 3 (2008):665-675,
https://doi.org/10.1002/jcp.21346 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1528 .