Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/10596
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dc.contributor.authorRadosavljevic, Gordana-
dc.contributor.authorVolarevic, Vladislav-
dc.contributor.authorJovanovic I.-
dc.contributor.authorMilovanovic, Marija-
dc.contributor.authorPejnović, Nada-
dc.contributor.authorArsenijevic, Nebojsa-
dc.contributor.authorHsu D.-
dc.contributor.authorLukic, Miodrag-
dc.date.accessioned2021-04-20T16:09:37Z-
dc.date.available2021-04-20T16:09:37Z-
dc.date.issued2012-
dc.identifier.issn0257-277X-
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/10596-
dc.description.abstractGalectin-3, a unique chimera-type member of the β-galactoside-binding soluble lectin family, is widely expressed in numerous cells. Here, we discuss the role of Galectin-3 in T-cell-mediated inflammatory (auto) immunity and tumor rejection by using Galectin-3-deficient mice and four disease models of human pathology: experimental autoimmune encephalomyelitis (EAE), Con-A-induced hepatitis, multiple low-dose streptozotocin-induced diabetes (MLD-STZ diabetes) and metastatic melanoma. We present evidence which suggest that Galectin-3 plays an important pro-inflammatory role in Con-A-induced hepatitis by promoting the activation of T lymphocytes, NKT cells and DCs, cytokine secretion, prevention of M2 macrophage polarization and apoptosis of mononuclear cells, and it leads to severe liver injury. In addition, experiments in Galectin-3-knock- out mice indicate that Galectin-3 is also involved in immune-mediated β-cell damage and is required for diabetogenesis in MLD-STZ model by promoting the expression of IFN-gamma, TNF-alpha, IL-17 and iNOS in immune and accessory effector cells. Next, our data demonstrated that Galectin-3 plays an important disease-exacerbating role in EAE through its multifunctional roles in preventing cell apoptosis and increasing IL-17 and IFN-gamma synthesis, but decreasing IL-10 production. Finally, based on our findings, we postulated that expression of Galectin-3 in the host may also facilitate melanoma metastasis by affecting tumor cell adhesion and modulating anti-melanoma immune response, in particular innate antitumor immunity. Taken together, we discuss the evidence of pro-inflammatory and antitumor activities of Galectin-3 and suggest that Galectin-3 may be an important therapeutic target. © 2012 Springer Science+Business Media, LLC.-
dc.rightsrestrictedAccess-
dc.sourceImmunologic Research-
dc.titleThe roles of Galectin-3 in autoimmunity and tumor progression-
dc.typereview-
dc.identifier.doi10.1007/s12026-012-8286-6-
dc.identifier.scopus2-s2.0-84859893633-
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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