TY  - JOUR
AU  - Cvjetičanin, Tamara
AU  - Miljković, Đorđe
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
AU  - Dekanski, Dragana P.
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1376
AB  - The health-promoting effects of various constituents of the olive tree (Olea europaea) are mainly associated with hypoglycaemic and insulin-sensitising activities and have been widely demonstrated in the metabolic syndrome and type 2 diabetes. However, their biological activity in autoimmune type I diabetes (TID) is poorly characterised. Therefore, the influence of O. europaea-derived components present in dry olive leaf extract (DOLE) was examined in two established preclinical models of human TID, which differ in some aspects of diabetogenesis: multiple low-dose streptozotocin-induced diabetes in susceptible C57BL/6 and CBA/H mouse strains; cyclophosphamide-accelerated diabetes in non-obese diabetic mice. In both T I D models, in vivo administration of DOLE significantly reduced clinical signs of diabetes (hyperglycaemia and body weight loss) and led to complete suppression of histopathological changes in pancreatic islets. In line with these, insulin expression and release were restored in DOLE-treated mice. Interestingly, inducible NO synthase expression and NO production were significantly elevated in peripheral tissues but were down-regulated within the local environment of the endocrine pancreas. This interference was reflected in NO-mediated suppression of T lymphocyte proliferation and lower production of the proinflammatory cytokines interferon-gamma, IL-17 and TNF-alpha in the spleen. with subsequent blockade of beta-cell destruction. The results suggest that DOLE interferes with development of autoimmune diabetes by down-regulating production of proinflammatory and cytotoxic mediators. Therefore, the potential use of a DOLE-enriched diet for prophylaxis/treatment of human T I D. and possibly other autoimmune diseases, is worthy of further investigation.
T2  - British Journal of Nutrition
T1  - Dried leaf extract of Olea europaea ameliorates islet-directed autoimmunity in mice
IS  - 10
VL  - 103
EP  - 1424
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1376
ER  - 

@article{
author = "Cvjetičanin, Tamara and Miljković, Đorđe and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava and Dekanski, Dragana P.",
year = "2010",
abstract = "The health-promoting effects of various constituents of the olive tree (Olea europaea) are mainly associated with hypoglycaemic and insulin-sensitising activities and have been widely demonstrated in the metabolic syndrome and type 2 diabetes. However, their biological activity in autoimmune type I diabetes (TID) is poorly characterised. Therefore, the influence of O. europaea-derived components present in dry olive leaf extract (DOLE) was examined in two established preclinical models of human TID, which differ in some aspects of diabetogenesis: multiple low-dose streptozotocin-induced diabetes in susceptible C57BL/6 and CBA/H mouse strains; cyclophosphamide-accelerated diabetes in non-obese diabetic mice. In both T I D models, in vivo administration of DOLE significantly reduced clinical signs of diabetes (hyperglycaemia and body weight loss) and led to complete suppression of histopathological changes in pancreatic islets. In line with these, insulin expression and release were restored in DOLE-treated mice. Interestingly, inducible NO synthase expression and NO production were significantly elevated in peripheral tissues but were down-regulated within the local environment of the endocrine pancreas. This interference was reflected in NO-mediated suppression of T lymphocyte proliferation and lower production of the proinflammatory cytokines interferon-gamma, IL-17 and TNF-alpha in the spleen. with subsequent blockade of beta-cell destruction. The results suggest that DOLE interferes with development of autoimmune diabetes by down-regulating production of proinflammatory and cytotoxic mediators. Therefore, the potential use of a DOLE-enriched diet for prophylaxis/treatment of human T I D. and possibly other autoimmune diseases, is worthy of further investigation.",
journal = "British Journal of Nutrition",
title = "Dried leaf extract of Olea europaea ameliorates islet-directed autoimmunity in mice",
number = "10",
volume = "103",
pages = "1424",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1376"
}

Cvjetičanin, T., Miljković, Đ., Stojanović, I. D., Stošić-Grujičić, S.,& Dekanski, D. P.. (2010). Dried leaf extract of Olea europaea ameliorates islet-directed autoimmunity in mice. in British Journal of Nutrition, 103(10).
https://hdl.handle.net/21.15107/rcub_ibiss_1376

Cvjetičanin T, Miljković Đ, Stojanović ID, Stošić-Grujičić S, Dekanski DP. Dried leaf extract of Olea europaea ameliorates islet-directed autoimmunity in mice. in British Journal of Nutrition. 2010;103(10):null-1424.
https://hdl.handle.net/21.15107/rcub_ibiss_1376 .

Cvjetičanin, Tamara, Miljković, Đorđe, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, Dekanski, Dragana P., "Dried leaf extract of Olea europaea ameliorates islet-directed autoimmunity in mice" in British Journal of Nutrition, 103, no. 10 (2010),
https://hdl.handle.net/21.15107/rcub_ibiss_1376 .

TY  - CONF
AU  - Stojanović, Ivana D.
AU  - Cvjetičanin, Tamara
AU  - Sandler, S
AU  - Stošić-Grujičić, Stanislava
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1347
C3  - Diabetologia
T1  - Deletion of macrophage migration inhibitory factor promotes obesity-associated insulin resistance while attenuating inflammation in mice fed a high-fat diet
IS  - null
VL  - 53
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1347
ER  - 

@conference{
author = "Stojanović, Ivana D. and Cvjetičanin, Tamara and Sandler, S and Stošić-Grujičić, Stanislava",
year = "2010",
journal = "Diabetologia",
title = "Deletion of macrophage migration inhibitory factor promotes obesity-associated insulin resistance while attenuating inflammation in mice fed a high-fat diet",
number = "null",
volume = "53",
pages = "na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1347"
}

Stojanović, I. D., Cvjetičanin, T., Sandler, S.,& Stošić-Grujičić, S.. (2010). Deletion of macrophage migration inhibitory factor promotes obesity-associated insulin resistance while attenuating inflammation in mice fed a high-fat diet. in Diabetologia, 53(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1347

Stojanović ID, Cvjetičanin T, Sandler S, Stošić-Grujičić S. Deletion of macrophage migration inhibitory factor promotes obesity-associated insulin resistance while attenuating inflammation in mice fed a high-fat diet. in Diabetologia. 2010;53(null):null-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1347 .

Stojanović, Ivana D., Cvjetičanin, Tamara, Sandler, S, Stošić-Grujičić, Stanislava, "Deletion of macrophage migration inhibitory factor promotes obesity-associated insulin resistance while attenuating inflammation in mice fed a high-fat diet" in Diabetologia, 53, no. null (2010),
https://hdl.handle.net/21.15107/rcub_ibiss_1347 .

TY  - CONF
AU  - Stošić-Grujičić, Stanislava
AU  - Cvjetičanin, Tamara
AU  - Timotijević, Gordana S
AU  - Zdravković, Nemanja S
AU  - Lukić, M
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1348
C3  - Diabetologia
T1  - Galectin-3 deficiency reduces immune-mediated beta cell destruction in vitro
IS  - null
VL  - 53
EP  - S209
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1348
ER  - 

@conference{
author = "Stošić-Grujičić, Stanislava and Cvjetičanin, Tamara and Timotijević, Gordana S and Zdravković, Nemanja S and Lukić, M",
year = "2010",
journal = "Diabetologia",
title = "Galectin-3 deficiency reduces immune-mediated beta cell destruction in vitro",
number = "null",
volume = "53",
pages = "S209",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1348"
}

Stošić-Grujičić, S., Cvjetičanin, T., Timotijević, G. S., Zdravković, N. S.,& Lukić, M.. (2010). Galectin-3 deficiency reduces immune-mediated beta cell destruction in vitro. in Diabetologia, 53(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1348

Stošić-Grujičić S, Cvjetičanin T, Timotijević GS, Zdravković NS, Lukić M. Galectin-3 deficiency reduces immune-mediated beta cell destruction in vitro. in Diabetologia. 2010;53(null):null-S209.
https://hdl.handle.net/21.15107/rcub_ibiss_1348 .

Stošić-Grujičić, Stanislava, Cvjetičanin, Tamara, Timotijević, Gordana S, Zdravković, Nemanja S, Lukić, M, "Galectin-3 deficiency reduces immune-mediated beta cell destruction in vitro" in Diabetologia, 53, no. null (2010),
https://hdl.handle.net/21.15107/rcub_ibiss_1348 .

TY  - CONF
AU  - Cvjetičanin, Tamara
AU  - Stošić-Grujičić, Stanislava
AU  - Sandler, S
AU  - Stojanović, Ivana D.
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1430
C3  - Diabetologia
T1  - The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes
IS  - null
VL  - 52
EP  - S246
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1430
ER  - 

@conference{
author = "Cvjetičanin, Tamara and Stošić-Grujičić, Stanislava and Sandler, S and Stojanović, Ivana D.",
year = "2009",
journal = "Diabetologia",
title = "The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes",
number = "null",
volume = "52",
pages = "S246",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1430"
}

Cvjetičanin, T., Stošić-Grujičić, S., Sandler, S.,& Stojanović, I. D.. (2009). The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes. in Diabetologia, 52(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1430

Cvjetičanin T, Stošić-Grujičić S, Sandler S, Stojanović ID. The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes. in Diabetologia. 2009;52(null):null-S246.
https://hdl.handle.net/21.15107/rcub_ibiss_1430 .

Cvjetičanin, Tamara, Stošić-Grujičić, Stanislava, Sandler, S, Stojanović, Ivana D., "The role of macrophage migration inhibitory factor in obesity-associated type 2 diabetes" in Diabetologia, 52, no. null (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1430 .

TY  - JOUR
AU  - Cvjetičanin, Tamara
AU  - Stojanović, Ivana D.
AU  - Timotijević, Gordana S
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1450
AB  - Background: Diabetes is characterized by progressive failure of insulin producing beta cells. It is well known that both saturated fatty acids and various products of immune cells can contribute to the reduction of beta cell viability and functionality during diabetes pathogenesis. However, their joint action on beta cells has not been investigated, so far. Therefore, we explored the possibility that leukocytes and saturated fatty acids cooperate in beta cell destruction. Results: Rat pancreatic islets or insulinoma cells (RIN) were co-cultivated with concanavalin A (ConA)-stimulated rat lymph node cells (LNC), or they were treated with cell-free supernatants (Sn) obtained from ConA-stimulated spleen cells or from activated CD3(+) cells, in the absence or presence of palmitic acid (PA). ConA-stimulated LNC or Sn and PA cooperated in inducing caspase-3-dependent RIN cell apoptosis. The observed effect of PA and Sn on RIN cell viability was mediated by p38 mitogen-activated protein kinase (MAPK)-signaling and was achieved through auto-destructive nitric oxide (NO) production. The cooperative effect of Sn was mimicked with the combination of interleukin-1 beta, interleukin-2, interleukin-6, interleukin-17, interferon-gamma and tumor necrosis factor-alpha. Conclusion: These results imply that stimulated T cells produce cytokines that cooperate with saturated free fatty acids in beta cell destruction during diabetes pathogenesis.
T2  - Bmc Immunology
T1  - T cells cooperate with palmitic acid in induction of beta cell apoptosis
IS  - null
VL  - 10
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1450
ER  - 

@article{
author = "Cvjetičanin, Tamara and Stojanović, Ivana D. and Timotijević, Gordana S and Stošić-Grujičić, Stanislava and Miljković, Đorđe",
year = "2009",
abstract = "Background: Diabetes is characterized by progressive failure of insulin producing beta cells. It is well known that both saturated fatty acids and various products of immune cells can contribute to the reduction of beta cell viability and functionality during diabetes pathogenesis. However, their joint action on beta cells has not been investigated, so far. Therefore, we explored the possibility that leukocytes and saturated fatty acids cooperate in beta cell destruction. Results: Rat pancreatic islets or insulinoma cells (RIN) were co-cultivated with concanavalin A (ConA)-stimulated rat lymph node cells (LNC), or they were treated with cell-free supernatants (Sn) obtained from ConA-stimulated spleen cells or from activated CD3(+) cells, in the absence or presence of palmitic acid (PA). ConA-stimulated LNC or Sn and PA cooperated in inducing caspase-3-dependent RIN cell apoptosis. The observed effect of PA and Sn on RIN cell viability was mediated by p38 mitogen-activated protein kinase (MAPK)-signaling and was achieved through auto-destructive nitric oxide (NO) production. The cooperative effect of Sn was mimicked with the combination of interleukin-1 beta, interleukin-2, interleukin-6, interleukin-17, interferon-gamma and tumor necrosis factor-alpha. Conclusion: These results imply that stimulated T cells produce cytokines that cooperate with saturated free fatty acids in beta cell destruction during diabetes pathogenesis.",
journal = "Bmc Immunology",
title = "T cells cooperate with palmitic acid in induction of beta cell apoptosis",
number = "null",
volume = "10",
pages = "na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1450"
}

Cvjetičanin, T., Stojanović, I. D., Timotijević, G. S., Stošić-Grujičić, S.,& Miljković, Đ.. (2009). T cells cooperate with palmitic acid in induction of beta cell apoptosis. in Bmc Immunology, 10(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1450

Cvjetičanin T, Stojanović ID, Timotijević GS, Stošić-Grujičić S, Miljković Đ. T cells cooperate with palmitic acid in induction of beta cell apoptosis. in Bmc Immunology. 2009;10(null):null-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1450 .

Cvjetičanin, Tamara, Stojanović, Ivana D., Timotijević, Gordana S, Stošić-Grujičić, Stanislava, Miljković, Đorđe, "T cells cooperate with palmitic acid in induction of beta cell apoptosis" in Bmc Immunology, 10, no. null (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1450 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Cvjetičanin, Tamara
AU  - Stojanović, Ivana D.
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1425
AB  - Retinoids have a variety of biological activities, including immunomodulatory action in a number of inflammatory and autoimmune conditions. Considering the pathogenesis of type 1 diabetes mellitus (T1D), in this study we examined the potential role for retinoids, etretinate and all-trans-retinoic acid (ATRA) in preclinical models of human T1D. When administered prophylactically to CBA/H mice made diabetic with multiple low doses of streptozotocin (MLD-STZ), both drugs effectively prevented clinical signs of diabetes. Prevention of T1D was associated with reduced emergence of primed (autoreactive) CD4(+) CD25(+) T cells, but not with the emergence of Foxp3(+) Treg in the peripheral compartments. Moreover, the animals receiving ATRA exhibited reduced Th1/Th17 response and nitric oxide (NO) production in the peripheral lymphoid tissues, thus shifting the balance towards the anti-inflammatory cytokines. In NOD mice with spontaneous form of diabetes, ATRA prophylaxis, starting at a time point immediately before T1D onset, markedly reduced hyperglycemia and incidence of the disease. However. administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. These findings suggest that effectiveness of T1D suppression by retinoids depends on the presence of Tregs which down-modulate immunoinflammatory events at the second "check-point" and allow diabetes progression. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Molecular Immunology
T1  - Retinoids differentially regulate the progression of autoimmune diabetes in three preclinical models in mice
IS  - 1
VL  - 47
EP  - 86
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1425
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Cvjetičanin, Tamara and Stojanović, Ivana D.",
year = "2009",
abstract = "Retinoids have a variety of biological activities, including immunomodulatory action in a number of inflammatory and autoimmune conditions. Considering the pathogenesis of type 1 diabetes mellitus (T1D), in this study we examined the potential role for retinoids, etretinate and all-trans-retinoic acid (ATRA) in preclinical models of human T1D. When administered prophylactically to CBA/H mice made diabetic with multiple low doses of streptozotocin (MLD-STZ), both drugs effectively prevented clinical signs of diabetes. Prevention of T1D was associated with reduced emergence of primed (autoreactive) CD4(+) CD25(+) T cells, but not with the emergence of Foxp3(+) Treg in the peripheral compartments. Moreover, the animals receiving ATRA exhibited reduced Th1/Th17 response and nitric oxide (NO) production in the peripheral lymphoid tissues, thus shifting the balance towards the anti-inflammatory cytokines. In NOD mice with spontaneous form of diabetes, ATRA prophylaxis, starting at a time point immediately before T1D onset, markedly reduced hyperglycemia and incidence of the disease. However. administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. These findings suggest that effectiveness of T1D suppression by retinoids depends on the presence of Tregs which down-modulate immunoinflammatory events at the second "check-point" and allow diabetes progression. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Molecular Immunology",
title = "Retinoids differentially regulate the progression of autoimmune diabetes in three preclinical models in mice",
number = "1",
volume = "47",
pages = "86",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1425"
}

Stošić-Grujičić, S., Cvjetičanin, T.,& Stojanović, I. D.. (2009). Retinoids differentially regulate the progression of autoimmune diabetes in three preclinical models in mice. in Molecular Immunology, 47(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1425

Stošić-Grujičić S, Cvjetičanin T, Stojanović ID. Retinoids differentially regulate the progression of autoimmune diabetes in three preclinical models in mice. in Molecular Immunology. 2009;47(1):null-86.
https://hdl.handle.net/21.15107/rcub_ibiss_1425 .

Stošić-Grujičić, Stanislava, Cvjetičanin, Tamara, Stojanović, Ivana D., "Retinoids differentially regulate the progression of autoimmune diabetes in three preclinical models in mice" in Molecular Immunology, 47, no. 1 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1425 .

TY  - CONF
AU  - Cvjetičanin, Tamara
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1515
C3  - Diabetologia
T1  - Does macrophage migration inhibitory factor precipitates obesity-associated type 2 diabetes development - an animal study
IS  - null
VL  - 51
EP  - S331
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1515
ER  - 

@conference{
author = "Cvjetičanin, Tamara and Stošić-Grujičić, Stanislava and Stojanović, Ivana D.",
year = "2008",
journal = "Diabetologia",
title = "Does macrophage migration inhibitory factor precipitates obesity-associated type 2 diabetes development - an animal study",
number = "null",
volume = "51",
pages = "S331",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1515"
}

Cvjetičanin, T., Stošić-Grujičić, S.,& Stojanović, I. D.. (2008). Does macrophage migration inhibitory factor precipitates obesity-associated type 2 diabetes development - an animal study. in Diabetologia, 51(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1515

Cvjetičanin T, Stošić-Grujičić S, Stojanović ID. Does macrophage migration inhibitory factor precipitates obesity-associated type 2 diabetes development - an animal study. in Diabetologia. 2008;51(null):null-S331.
https://hdl.handle.net/21.15107/rcub_ibiss_1515 .

Cvjetičanin, Tamara, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., "Does macrophage migration inhibitory factor precipitates obesity-associated type 2 diabetes development - an animal study" in Diabetologia, 51, no. null (2008),
https://hdl.handle.net/21.15107/rcub_ibiss_1515 .