Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/10409
Title: ST2 gene-deletion reveals a role of Foxp3<sup>+</sup> regulatory T cells in diabetes modulation in BALB/c mice
Authors: Zdravkovic, Nemanja
Pavlovic D.
Zdravkovic, Vladimir
Pejnović, Nada
Arsenijevic, Nebojsa
Lukic, Miodrag
Journal: Translational Research
Issue Date: 1-Jan-2013
Abstract: BALB/c mice are resistant to diabetes induced by multiple low doses of streptozotocin (MLD-STZ; 5 × 40 mg/kg body weight [b.w.]) regimen in contrast to C57/BL6 mice. The deletion of ST2 gene renders BALB/c mice susceptible to diabetes induction. Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice. We argued that a lower dose of CY may selectively eliminate Tregs while sparing effector T cells in BALB/c mice. Indeed, only a very low dose of CY (50 mg/kg b.w.) enhanced diabetes severity in ST2KO mice. This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF- α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata. Also, the aggravation of diabetes was accompanied with increased serum levels of TNF-α, IFN-γ, and IL-17. Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3 + regulatory T cells in the pancreatic lymph nodes in diabetes modulation. © 2013 Mosby, Inc. All rights reserved.
URI: https://scidar.kg.ac.rs/handle/123456789/10409
Type: journal article
DOI: 10.1016/j.trsl.2012.10.005
ISSN: 19315244
SCOPUS: 84872378799
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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