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Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus.
J Cell Physiol. 2008 Jun; 215(3):665-75.JC

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 1 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-1beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, 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(-/-) 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.

Authors+Show Affiliations

Department of Immunology, Institute for Biological Research Sinisa Stankovic, Belgrade, Serbia. duta@eunet.yuNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18064633

Citation

Stosic-Grujicic, Stanislava, et al. "Macrophage Migration Inhibitory Factor (MIF) Is Necessary for Progression of Autoimmune Diabetes Mellitus." Journal of Cellular Physiology, vol. 215, no. 3, 2008, pp. 665-75.
Stosic-Grujicic S, Stojanovic I, Maksimovic-Ivanic D, et al. Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. J Cell Physiol. 2008;215(3):665-75.
Stosic-Grujicic, S., Stojanovic, I., Maksimovic-Ivanic, D., Momcilovic, M., Popadic, D., Harhaji, L., Miljkovic, D., 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. Journal of Cellular Physiology, 215(3), 665-75.
Stosic-Grujicic S, et al. Macrophage Migration Inhibitory Factor (MIF) Is Necessary for Progression of Autoimmune Diabetes Mellitus. J Cell Physiol. 2008;215(3):665-75. PubMed PMID: 18064633.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. AU - Stosic-Grujicic,Stanislava, AU - Stojanovic,Ivana, AU - Maksimovic-Ivanic,Danijela, AU - Momcilovic,Miljana, AU - Popadic,Dusan, AU - Harhaji,Ljubica, AU - Miljkovic,Djordje, AU - Metz,Christine, AU - Mangano,Katia, AU - Papaccio,Gianpaolo, AU - Al-Abed,Yousef, AU - Nicoletti,Ferdinando, PY - 2007/12/8/pubmed PY - 2008/4/30/medline PY - 2007/12/8/entrez SP - 665 EP - 75 JF - Journal of cellular physiology JO - J Cell Physiol VL - 215 IS - 3 N2 - 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 1 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-1beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, 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(-/-) 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. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/18064633/Macrophage_migration_inhibitory_factor__MIF__is_necessary_for_progression_of_autoimmune_diabetes_mellitus_ DB - PRIME DP - Unbound Medicine ER -