TY  - JOUR
AU  - Radović, Julijana M
AU  - Maksimović-Ivanić, Danijela
AU  - Timotijević, Gordana S
AU  - Popadić, S
AU  - Ramić, Zorica D.
AU  - Trajković, Vladimir S
AU  - Miljković, Đorđe
AU  - Stošić-Grujičić, Stanislava
AU  - Mijatović, Sanja
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1135
AB  - Intrinsic characteristics of melanoma cells such as expression of inducible nitric oxide synthase (iNOS), redox status, and activity of signaling pathways involved in proliferation, differentiation and cell death define the response of the cells to the diverse treatments. In this context we compared the effectiveness of herbal antaquinone aloe emodin (AE) against mouse B16 melanoma and human A375, different in initial activity of ERK1/2, constitutive iNOS expression and basal level of reactive oxygen species (ROS). Both cell lines are sensitive to AE treatment. However, while the agent induces differentiation of B16 cells toward melanocytes, in A375 cells promoted massive apoptosis. Differentiation of B16 cells, characterized by enhanced melanin production and tyrosinase activity, was mediated by H2O2 production synchronized with rapid p53 accumulation and enhanced expression of cyclins D1 and D3. Caspase mediated apoptosis triggered in A375 cells was accompanied with Bcl-2 but not iNOS down-regulation. In addition, opposite regulation of Akt-ERK1/2 axis in AE treated B16 and A375 cells correlated with different outcome of the treatment. However, AE in a dose-dependent manner rescued both B16 and A375 cells from doxorubicin- or paclitaxel-induced killing. These data indicate that caution is warranted when AE is administrated to the patients with conventional chemotherapy. (C) 2012 Elsevier Ltd. All rights reserved.
T2  - Food and Chemical Toxicology
T1  - Cell-type dependent response of melanoma cells to aloe emodin
IS  - 9
VL  - 50
SP  - 911
EP  - 3189
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1135
ER  - 

@article{
author = "Radović, Julijana M and Maksimović-Ivanić, Danijela and Timotijević, Gordana S and Popadić, S and Ramić, Zorica D. and Trajković, Vladimir S and Miljković, Đorđe and Stošić-Grujičić, Stanislava and Mijatović, Sanja",
year = "2012",
abstract = "Intrinsic characteristics of melanoma cells such as expression of inducible nitric oxide synthase (iNOS), redox status, and activity of signaling pathways involved in proliferation, differentiation and cell death define the response of the cells to the diverse treatments. In this context we compared the effectiveness of herbal antaquinone aloe emodin (AE) against mouse B16 melanoma and human A375, different in initial activity of ERK1/2, constitutive iNOS expression and basal level of reactive oxygen species (ROS). Both cell lines are sensitive to AE treatment. However, while the agent induces differentiation of B16 cells toward melanocytes, in A375 cells promoted massive apoptosis. Differentiation of B16 cells, characterized by enhanced melanin production and tyrosinase activity, was mediated by H2O2 production synchronized with rapid p53 accumulation and enhanced expression of cyclins D1 and D3. Caspase mediated apoptosis triggered in A375 cells was accompanied with Bcl-2 but not iNOS down-regulation. In addition, opposite regulation of Akt-ERK1/2 axis in AE treated B16 and A375 cells correlated with different outcome of the treatment. However, AE in a dose-dependent manner rescued both B16 and A375 cells from doxorubicin- or paclitaxel-induced killing. These data indicate that caution is warranted when AE is administrated to the patients with conventional chemotherapy. (C) 2012 Elsevier Ltd. All rights reserved.",
journal = "Food and Chemical Toxicology",
title = "Cell-type dependent response of melanoma cells to aloe emodin",
number = "9",
volume = "50",
pages = "911-3189",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1135"
}

Radović, J. M., Maksimović-Ivanić, D., Timotijević, G. S., Popadić, S., Ramić, Z. D., Trajković, V. S., Miljković, Đ., Stošić-Grujičić, S.,& Mijatović, S.. (2012). Cell-type dependent response of melanoma cells to aloe emodin. in Food and Chemical Toxicology, 50(9), 911-3189.
https://hdl.handle.net/21.15107/rcub_ibiss_1135

Radović JM, Maksimović-Ivanić D, Timotijević GS, Popadić S, Ramić ZD, Trajković VS, Miljković Đ, Stošić-Grujičić S, Mijatović S. Cell-type dependent response of melanoma cells to aloe emodin. in Food and Chemical Toxicology. 2012;50(9):911-3189.
https://hdl.handle.net/21.15107/rcub_ibiss_1135 .

Radović, Julijana M, Maksimović-Ivanić, Danijela, Timotijević, Gordana S, Popadić, S, Ramić, Zorica D., Trajković, Vladimir S, Miljković, Đorđe, Stošić-Grujičić, Stanislava, Mijatović, Sanja, "Cell-type dependent response of melanoma cells to aloe emodin" in Food and Chemical Toxicology, 50, no. 9 (2012):911-3189,
https://hdl.handle.net/21.15107/rcub_ibiss_1135 .

TY  - JOUR
AU  - Marković, Milos
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Popadić, Dusan M
AU  - Miljković, Zeljka
AU  - Savić, Emina
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1129
AB  - Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Molecular Immunology
T1  - Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles
IS  - 1
VL  - 47
SP  - 243
EP  - 146
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1129
ER  - 

@article{
author = "Marković, Milos and Miljković, Đorđe and Momčilović, Miljana and Popadić, Dusan M and Miljković, Zeljka and Savić, Emina and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Molecular Immunology",
title = "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles",
number = "1",
volume = "47",
pages = "243-146",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1129"
}

Marković, M., Miljković, Đ., Momčilović, M., Popadić, D. M., Miljković, Z., Savić, E., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2009). Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology, 47(1), 243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129

Marković M, Miljković Đ, Momčilović M, Popadić DM, Miljković Z, Savić E, Ramić ZD, Mostarica-Stojković MB. Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology. 2009;47(1):243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

Marković, Milos, Miljković, Đorđe, Momčilović, Miljana, Popadić, Dusan M, Miljković, Zeljka, Savić, Emina, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles" in Molecular Immunology, 47, no. 1 (2009):243-146,
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

TY  - JOUR
AU  - Momčilović, Miljana
AU  - Miljković, Zeljka
AU  - Popadić, Dusan M
AU  - Marković, Milos
AU  - Savić, Emina
AU  - Ramić, Zorica D.
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1519
AB  - Background: Interleukin-17 (IL-17)-producing cells are increasingly considered to be the major pathogenic population in various autoimmune disorders. The effects of glucocorticoids, widely used as therapeutics for inflammatory and autoimmune disorders, on IL-17 generation have not been thoroughly investigated so far. Therefore, we have explored the influence of methylprednisolone (MP) on IL-17 expression in rat lymphocytes, and compared it to the effect of the drug on interferon (IFN)-gamma. Results: Production of IL-17 in mitogen-stimulated lymph node cells (LNC) from non-treated rats, as well as in myelin basic protein (MBP)-stimulated draining LNC from rats immunized with spinal cord homogenate and complete Freund's adjuvant was significantly reduced by MP. The reduction was dose-dependent, sustained through the follow-up period of 48 hours, and was not achieved through anti-proliferative effect. Additionally, MP inhibited IL-17 production in purified T cells as well, but to less extent than in LNC. In its influence on IL-17 production MP inhibited Ror-gamma T transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-gamma in inhibiting IL-17 generation in LNC. Conclusion: The observed difference in the effect of MP on IL-17 and IFN-gamma could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.
T2  - Bmc Immunology
T1  - Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells
IS  - null
VL  - 9
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1519
ER  - 

@article{
author = "Momčilović, Miljana and Miljković, Zeljka and Popadić, Dusan M and Marković, Milos and Savić, Emina and Ramić, Zorica D. and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2008",
abstract = "Background: Interleukin-17 (IL-17)-producing cells are increasingly considered to be the major pathogenic population in various autoimmune disorders. The effects of glucocorticoids, widely used as therapeutics for inflammatory and autoimmune disorders, on IL-17 generation have not been thoroughly investigated so far. Therefore, we have explored the influence of methylprednisolone (MP) on IL-17 expression in rat lymphocytes, and compared it to the effect of the drug on interferon (IFN)-gamma. Results: Production of IL-17 in mitogen-stimulated lymph node cells (LNC) from non-treated rats, as well as in myelin basic protein (MBP)-stimulated draining LNC from rats immunized with spinal cord homogenate and complete Freund's adjuvant was significantly reduced by MP. The reduction was dose-dependent, sustained through the follow-up period of 48 hours, and was not achieved through anti-proliferative effect. Additionally, MP inhibited IL-17 production in purified T cells as well, but to less extent than in LNC. In its influence on IL-17 production MP inhibited Ror-gamma T transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-gamma in inhibiting IL-17 generation in LNC. Conclusion: The observed difference in the effect of MP on IL-17 and IFN-gamma could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.",
journal = "Bmc Immunology",
title = "Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells",
number = "null",
volume = "9",
pages = "na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1519"
}

Momčilović, M., Miljković, Z., Popadić, D. M., Marković, M., Savić, E., Ramić, Z. D., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2008). Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells. in Bmc Immunology, 9(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1519

Momčilović M, Miljković Z, Popadić DM, Marković M, Savić E, Ramić ZD, Miljković Đ, Mostarica-Stojković MB. Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells. in Bmc Immunology. 2008;9(null):null-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1519 .

Momčilović, Miljana, Miljković, Zeljka, Popadić, Dusan M, Marković, Milos, Savić, Emina, Ramić, Zorica D., Miljković, Đorđe, Mostarica-Stojković, Marija B, "Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells" in Bmc Immunology, 9, no. null (2008),
https://hdl.handle.net/21.15107/rcub_ibiss_1519 .

TY  - JOUR
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
AU  - Ramić, Zorica D.
AU  - Momčilović, Miljana
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1568
AB  - Astrocytes play important roles in the complex and as yet not very well understood net of interactions among resident and infiltrating cells during central nervous system (CNS) inflammation. In such an intricate network, cytokines represent an essential means for intercellular communication, and astrocytes are able to affect their generation and/or release. Among various cytokines produced by infiltrating cells, interferon (IFN)-gamma and interleukin (IL)-17 are the focus of this research, because they are pivotal cytokines of helper T-cell type 1 (Th1) and helper T-cell type 17 (Th17), respectively. Importantly, both Th1 and Th17 cells, as well as their cytokines, have been shown to be of importance for the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of a prototypical CNS disease with inflammatory pathogenesis, multiple sclerosis. Therefore, the influence of astrocytes on the generation of IFN-gamma and IL-17 in concanavalin A- and myelin basic protein-stimulated lymph node cells of healthy rats and rats with developing EAE, respectively, was investigated in vitro. Astrocytes up-regulated IL-17 and IFN-gamma gene expression and protein synthesis in T cells, which coincided with astrocytes' ability to express IL-23 subunit p19 and common IL-12/IL-23 subunit p40 but not IL-12 subunit p35 in the cocultivations. These results suggest one more way in which astrocytes could contribute to the complex interactions during CNS inflammation. (C) 2007 Wiley-Liss, Inc.
T2  - Journal of Neuroscience Research
T1  - Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro
IS  - 16
VL  - 85
EP  - 3606
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1568
ER  - 

@article{
author = "Stojanović, Ivana D. and Stošić-Grujičić, Stanislava and Ramić, Zorica D. and Momčilović, Miljana and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2007",
abstract = "Astrocytes play important roles in the complex and as yet not very well understood net of interactions among resident and infiltrating cells during central nervous system (CNS) inflammation. In such an intricate network, cytokines represent an essential means for intercellular communication, and astrocytes are able to affect their generation and/or release. Among various cytokines produced by infiltrating cells, interferon (IFN)-gamma and interleukin (IL)-17 are the focus of this research, because they are pivotal cytokines of helper T-cell type 1 (Th1) and helper T-cell type 17 (Th17), respectively. Importantly, both Th1 and Th17 cells, as well as their cytokines, have been shown to be of importance for the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of a prototypical CNS disease with inflammatory pathogenesis, multiple sclerosis. Therefore, the influence of astrocytes on the generation of IFN-gamma and IL-17 in concanavalin A- and myelin basic protein-stimulated lymph node cells of healthy rats and rats with developing EAE, respectively, was investigated in vitro. Astrocytes up-regulated IL-17 and IFN-gamma gene expression and protein synthesis in T cells, which coincided with astrocytes' ability to express IL-23 subunit p19 and common IL-12/IL-23 subunit p40 but not IL-12 subunit p35 in the cocultivations. These results suggest one more way in which astrocytes could contribute to the complex interactions during CNS inflammation. (C) 2007 Wiley-Liss, Inc.",
journal = "Journal of Neuroscience Research",
title = "Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro",
number = "16",
volume = "85",
pages = "3606",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1568"
}

Stojanović, I. D., Stošić-Grujičić, S., Ramić, Z. D., Momčilović, M., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2007). Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro. in Journal of Neuroscience Research, 85(16).
https://hdl.handle.net/21.15107/rcub_ibiss_1568

Stojanović ID, Stošić-Grujičić S, Ramić ZD, Momčilović M, Miljković Đ, Mostarica-Stojković MB. Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro. in Journal of Neuroscience Research. 2007;85(16):null-3606.
https://hdl.handle.net/21.15107/rcub_ibiss_1568 .

Stojanović, Ivana D., Stošić-Grujičić, Stanislava, Ramić, Zorica D., Momčilović, Miljana, Miljković, Đorđe, Mostarica-Stojković, Marija B, "Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro" in Journal of Neuroscience Research, 85, no. 16 (2007),
https://hdl.handle.net/21.15107/rcub_ibiss_1568 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Stošić-Grujičić, Stanislava
AU  - Marković, Miloš
AU  - Momčilović, Miljana
AU  - Ramić, Zorica D.
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Popadić, Dusan M
AU  - Stojanović, Ivana D.
AU  - Mostarica-Stojković, Marija B
PY  - 2006
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1641
AB  - Albino Oxford (AO) rats, unlike Dark Agouti (DA) rats are resistant to the induction of experimental autoimmune encephalomyelitis (EAE). The reason for the resistance could be some restraining mechanism preventing auto-aggressive cell activation at the level of draining lymph nodes (DLN) during the induction phase of the disease. Such a mechanism could be anti-proliferative action of nitric oxide (NO), which has already been shown of importance for the resistance of several rat strains to the induction of the disease. Importantly, number of AO DLN cells (DLNC) is markedly lower and with lower proliferative response to myelin basic protein (MBP) ex vivo in comparison to DA DLNC in the inductive phase of EAE, thus implying that in AO rats DLNC do not proliferate as extensively as in DA rats. We show that AO rats do not produce larger quantities of NO than DA rats after immunization. Further, DLNC of immunized AO rats have significantly lower mRNA expression and synthesis of interferon (IFN)-gamma and interleukin (IL)-17 compared to DLNC of DA rats. Collectively, these results suggest that there is a substantial difference between EAE-resistant AO rats and EAE-prone DA rats in the initiation of autoimmune response. This difference seems to be independent of anti- proliferative actions of NO, but correlates with impaired IL-17 production in AO rats. (c) 2006 Wiley-Liss, Inc.
T2  - Journal of Neuroscience Research
T1  - Strain difference in susceptibility to experimental autoimmune encephalomyelitis between albino oxford and dark agouti rats correlates with disparity in production of IL-17, but not nitric oxide
IS  - 2
VL  - 84
DO  - 10.1002/jnr.20883
SP  - 237
EP  - 388
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1641
ER  - 

@article{
author = "Miljković, Đorđe and Stošić-Grujičić, Stanislava and Marković, Miloš and Momčilović, Miljana and Ramić, Zorica D. and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Popadić, Dusan M and Stojanović, Ivana D. and Mostarica-Stojković, Marija B",
year = "2006",
abstract = "Albino Oxford (AO) rats, unlike Dark Agouti (DA) rats are resistant to the induction of experimental autoimmune encephalomyelitis (EAE). The reason for the resistance could be some restraining mechanism preventing auto-aggressive cell activation at the level of draining lymph nodes (DLN) during the induction phase of the disease. Such a mechanism could be anti-proliferative action of nitric oxide (NO), which has already been shown of importance for the resistance of several rat strains to the induction of the disease. Importantly, number of AO DLN cells (DLNC) is markedly lower and with lower proliferative response to myelin basic protein (MBP) ex vivo in comparison to DA DLNC in the inductive phase of EAE, thus implying that in AO rats DLNC do not proliferate as extensively as in DA rats. We show that AO rats do not produce larger quantities of NO than DA rats after immunization. Further, DLNC of immunized AO rats have significantly lower mRNA expression and synthesis of interferon (IFN)-gamma and interleukin (IL)-17 compared to DLNC of DA rats. Collectively, these results suggest that there is a substantial difference between EAE-resistant AO rats and EAE-prone DA rats in the initiation of autoimmune response. This difference seems to be independent of anti- proliferative actions of NO, but correlates with impaired IL-17 production in AO rats. (c) 2006 Wiley-Liss, Inc.",
journal = "Journal of Neuroscience Research",
title = "Strain difference in susceptibility to experimental autoimmune encephalomyelitis between albino oxford and dark agouti rats correlates with disparity in production of IL-17, but not nitric oxide",
number = "2",
volume = "84",
doi = "10.1002/jnr.20883",
pages = "237-388",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1641"
}

Miljković, Đ., Stošić-Grujičić, S., Marković, M., Momčilović, M., Ramić, Z. D., Maksimović-Ivanić, D., Mijatović, S., Popadić, D. M., Stojanović, I. D.,& Mostarica-Stojković, M. B.. (2006). Strain difference in susceptibility to experimental autoimmune encephalomyelitis between albino oxford and dark agouti rats correlates with disparity in production of IL-17, but not nitric oxide. in Journal of Neuroscience Research, 84(2), 237-388.
https://doi.org/10.1002/jnr.20883
https://hdl.handle.net/21.15107/rcub_ibiss_1641

Miljković Đ, Stošić-Grujičić S, Marković M, Momčilović M, Ramić ZD, Maksimović-Ivanić D, Mijatović S, Popadić DM, Stojanović ID, Mostarica-Stojković MB. Strain difference in susceptibility to experimental autoimmune encephalomyelitis between albino oxford and dark agouti rats correlates with disparity in production of IL-17, but not nitric oxide. in Journal of Neuroscience Research. 2006;84(2):237-388.
doi:10.1002/jnr.20883
https://hdl.handle.net/21.15107/rcub_ibiss_1641 .

Miljković, Đorđe, Stošić-Grujičić, Stanislava, Marković, Miloš, Momčilović, Miljana, Ramić, Zorica D., Maksimović-Ivanić, Danijela, Mijatović, Sanja, Popadić, Dusan M, Stojanović, Ivana D., Mostarica-Stojković, Marija B, "Strain difference in susceptibility to experimental autoimmune encephalomyelitis between albino oxford and dark agouti rats correlates with disparity in production of IL-17, but not nitric oxide" in Journal of Neuroscience Research, 84, no. 2 (2006):237-388,
https://doi.org/10.1002/jnr.20883 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1641 .

TY  - CONF
AU  - Marković, Milos
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Stošić-Grujičić, Stanislava
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2006
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1635
C3  - Journal of Neuroimmunology
T1  - Differential regulation of IL-12 IFN-gamma and IL-23 IL-17 axes might account for discrepancy in susceptibility towards experimental autoimmune encephalomyelitis between Albino Oxford and Dark Agouti rats
IS  - null
VL  - 178
EP  - 51
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1635
ER  - 

@conference{
author = "Marković, Milos and Miljković, Đorđe and Momčilović, Miljana and Stošić-Grujičić, Stanislava and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2006",
journal = "Journal of Neuroimmunology",
title = "Differential regulation of IL-12 IFN-gamma and IL-23 IL-17 axes might account for discrepancy in susceptibility towards experimental autoimmune encephalomyelitis between Albino Oxford and Dark Agouti rats",
number = "null",
volume = "178",
pages = "51",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1635"
}

Marković, M., Miljković, Đ., Momčilović, M., Stošić-Grujičić, S., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2006). Differential regulation of IL-12 IFN-gamma and IL-23 IL-17 axes might account for discrepancy in susceptibility towards experimental autoimmune encephalomyelitis between Albino Oxford and Dark Agouti rats. in Journal of Neuroimmunology, 178(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1635

Marković M, Miljković Đ, Momčilović M, Stošić-Grujičić S, Ramić ZD, Mostarica-Stojković MB. Differential regulation of IL-12 IFN-gamma and IL-23 IL-17 axes might account for discrepancy in susceptibility towards experimental autoimmune encephalomyelitis between Albino Oxford and Dark Agouti rats. in Journal of Neuroimmunology. 2006;178(null):null-51.
https://hdl.handle.net/21.15107/rcub_ibiss_1635 .

Marković, Milos, Miljković, Đorđe, Momčilović, Miljana, Stošić-Grujičić, Stanislava, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Differential regulation of IL-12 IFN-gamma and IL-23 IL-17 axes might account for discrepancy in susceptibility towards experimental autoimmune encephalomyelitis between Albino Oxford and Dark Agouti rats" in Journal of Neuroimmunology, 178, no. null (2006),
https://hdl.handle.net/21.15107/rcub_ibiss_1635 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Ramić, Zorica D.
AU  - Bumbaširević, Vesna D
AU  - Harhaji-Trajković, Ljubica
AU  - Mostarica-Stojković, Marija B
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1736
AB  - Experimental autoimmune encephalomyelitis (EAE) is a well-recognized model for multiple sclerosis (MS) in humans. However, adjuvants used with encephalitogens to induce EAE produce non-specific effects interfering with the mechanisms involved in the autoimmune response to the central nervous system (CNS) tissue. It is therefore important to establish a more suitable model of EAE for analysis of autoimmune phenomena resembling those operative in MS. Here we report that EAE can be induced regularly in Dark Agouti (DA) strain of rats with spinal cord tissue without any adjuvant, as judged by both clinical and histological parameters. The incidence and severity of EAE depended on the origin of the encephalitogen, the rat versus guinea pig spinal cord homogenate being more efficient. Furthermore, EAE could be reinduced in animals which had recovered from disease that had been induced actively with encephalitogen alone, suggesting the role of adjuvant-generated non-specific mechanisms in resistance to reinduction of EAE. Thus, EAE induced in DA rats with encephalitogen alone provides a reproducible model for defining pathogenically relevant events in CNS autoimmunity devoid of the potentially misleading effects of adjuvants.
T2  - Clinical and Experimental Immunology
T1  - Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant
IS  - 1
VL  - 136
EP  - 55
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1736
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Ramić, Zorica D. and Bumbaširević, Vesna D and Harhaji-Trajković, Ljubica and Mostarica-Stojković, Marija B",
year = "2004",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is a well-recognized model for multiple sclerosis (MS) in humans. However, adjuvants used with encephalitogens to induce EAE produce non-specific effects interfering with the mechanisms involved in the autoimmune response to the central nervous system (CNS) tissue. It is therefore important to establish a more suitable model of EAE for analysis of autoimmune phenomena resembling those operative in MS. Here we report that EAE can be induced regularly in Dark Agouti (DA) strain of rats with spinal cord tissue without any adjuvant, as judged by both clinical and histological parameters. The incidence and severity of EAE depended on the origin of the encephalitogen, the rat versus guinea pig spinal cord homogenate being more efficient. Furthermore, EAE could be reinduced in animals which had recovered from disease that had been induced actively with encephalitogen alone, suggesting the role of adjuvant-generated non-specific mechanisms in resistance to reinduction of EAE. Thus, EAE induced in DA rats with encephalitogen alone provides a reproducible model for defining pathogenically relevant events in CNS autoimmunity devoid of the potentially misleading effects of adjuvants.",
journal = "Clinical and Experimental Immunology",
title = "Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant",
number = "1",
volume = "136",
pages = "55",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1736"
}

Stošić-Grujičić, S., Ramić, Z. D., Bumbaširević, V. D., Harhaji-Trajković, L.,& Mostarica-Stojković, M. B.. (2004). Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant. in Clinical and Experimental Immunology, 136(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1736

Stošić-Grujičić S, Ramić ZD, Bumbaširević VD, Harhaji-Trajković L, Mostarica-Stojković MB. Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant. in Clinical and Experimental Immunology. 2004;136(1):null-55.
https://hdl.handle.net/21.15107/rcub_ibiss_1736 .

Stošić-Grujičić, Stanislava, Ramić, Zorica D., Bumbaširević, Vesna D, Harhaji-Trajković, Ljubica, Mostarica-Stojković, Marija B, "Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant" in Clinical and Experimental Immunology, 136, no. 1 (2004),
https://hdl.handle.net/21.15107/rcub_ibiss_1736 .

TY  - CONF
AU  - Popadić, Dusan M
AU  - Ljubić, J
AU  - Vucković, Olivera
AU  - Harhaji-Trajković, Ljubica
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1728
C3  - Journal of Neuroimmunology
T1  - Mononuclear cells from infiltrating spinal cords of rats with EAE suppress mitogen induced T cell proliferation in vitro
IS  - 1-2
VL  - 154
EP  - 61
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1728
ER  - 

@conference{
author = "Popadić, Dusan M and Ljubić, J and Vucković, Olivera and Harhaji-Trajković, Ljubica and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2004",
journal = "Journal of Neuroimmunology",
title = "Mononuclear cells from infiltrating spinal cords of rats with EAE suppress mitogen induced T cell proliferation in vitro",
number = "1-2",
volume = "154",
pages = "61",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1728"
}

Popadić, D. M., Ljubić, J., Vucković, O., Harhaji-Trajković, L., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2004). Mononuclear cells from infiltrating spinal cords of rats with EAE suppress mitogen induced T cell proliferation in vitro. in Journal of Neuroimmunology, 154(1-2).
https://hdl.handle.net/21.15107/rcub_ibiss_1728

Popadić DM, Ljubić J, Vucković O, Harhaji-Trajković L, Ramić ZD, Mostarica-Stojković MB. Mononuclear cells from infiltrating spinal cords of rats with EAE suppress mitogen induced T cell proliferation in vitro. in Journal of Neuroimmunology. 2004;154(1-2):null-61.
https://hdl.handle.net/21.15107/rcub_ibiss_1728 .

Popadić, Dusan M, Ljubić, J, Vucković, Olivera, Harhaji-Trajković, Ljubica, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Mononuclear cells from infiltrating spinal cords of rats with EAE suppress mitogen induced T cell proliferation in vitro" in Journal of Neuroimmunology, 154, no. 1-2 (2004),
https://hdl.handle.net/21.15107/rcub_ibiss_1728 .

TY  - JOUR
AU  - Trajković, Vladimir S
AU  - Vucković, Olivera
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
AU  - Popadić, Dušan M.
AU  - Marković, Miloš
AU  - Bumbaširević, Vesna D
AU  - Backović, Aleksandar
AU  - Stojanović, Ivana D.
AU  - Harhaji-Trajković, Ljubica
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1682
AB  - Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.
T2  - Glia
T1  - Astrocyte-induced regulatory T cells mitigate CNS autoimmunity
IS  - 2
VL  - 47
DO  - 10.1002/glia.20046
SP  - 168
EP  - 179
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1682
ER  - 

@article{
author = "Trajković, Vladimir S and Vucković, Olivera and Stošić-Grujičić, Stanislava and Miljković, Đorđe and Popadić, Dušan M. and Marković, Miloš and Bumbaširević, Vesna D and Backović, Aleksandar and Stojanović, Ivana D. and Harhaji-Trajković, Ljubica and Ramić, Zorica D. and Mostarica-Stojković, Marija",
year = "2004",
abstract = "Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.",
journal = "Glia",
title = "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity",
number = "2",
volume = "47",
doi = "10.1002/glia.20046",
pages = "168-179",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1682"
}

Trajković, V. S., Vucković, O., Stošić-Grujičić, S., Miljković, Đ., Popadić, D. M., Marković, M., Bumbaširević, V. D., Backović, A., Stojanović, I. D., Harhaji-Trajković, L., Ramić, Z. D.,& Mostarica-Stojković, M.. (2004). Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia, 47(2), 168-179.
https://doi.org/10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682

Trajković VS, Vucković O, Stošić-Grujičić S, Miljković Đ, Popadić DM, Marković M, Bumbaširević VD, Backović A, Stojanović ID, Harhaji-Trajković L, Ramić ZD, Mostarica-Stojković M. Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia. 2004;47(2):168-179.
doi:10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .

Trajković, Vladimir S, Vucković, Olivera, Stošić-Grujičić, Stanislava, Miljković, Đorđe, Popadić, Dušan M., Marković, Miloš, Bumbaširević, Vesna D, Backović, Aleksandar, Stojanović, Ivana D., Harhaji-Trajković, Ljubica, Ramić, Zorica D., Mostarica-Stojković, Marija, "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity" in Glia, 47, no. 2 (2004):168-179,
https://doi.org/10.1002/glia.20046 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .

TY  - CONF
AU  - Marković, Milos
AU  - Vucković, Olivera
AU  - Trajković, Vladimir S
AU  - Stošić-Grujičić, Stanislava
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1729
C3  - Journal of Neuroimmunology
T1  - Astrocyte-induced regulatory T cells suppress EAE in DA rats
IS  - 1-2
VL  - 154
EP  - 80
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1729
ER  - 

@conference{
author = "Marković, Milos and Vucković, Olivera and Trajković, Vladimir S and Stošić-Grujičić, Stanislava and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2004",
journal = "Journal of Neuroimmunology",
title = "Astrocyte-induced regulatory T cells suppress EAE in DA rats",
number = "1-2",
volume = "154",
pages = "80",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1729"
}

Marković, M., Vucković, O., Trajković, V. S., Stošić-Grujičić, S., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2004). Astrocyte-induced regulatory T cells suppress EAE in DA rats. in Journal of Neuroimmunology, 154(1-2).
https://hdl.handle.net/21.15107/rcub_ibiss_1729

Marković M, Vucković O, Trajković VS, Stošić-Grujičić S, Ramić ZD, Mostarica-Stojković MB. Astrocyte-induced regulatory T cells suppress EAE in DA rats. in Journal of Neuroimmunology. 2004;154(1-2):null-80.
https://hdl.handle.net/21.15107/rcub_ibiss_1729 .

Marković, Milos, Vucković, Olivera, Trajković, Vladimir S, Stošić-Grujičić, Stanislava, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Astrocyte-induced regulatory T cells suppress EAE in DA rats" in Journal of Neuroimmunology, 154, no. 1-2 (2004),
https://hdl.handle.net/21.15107/rcub_ibiss_1729 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Savić-Radojević, Ana R
AU  - Maksimović-Ivanić, Danijela
AU  - Marković, Milos
AU  - Bumbaširević, Vesna D
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1788
AB  - The immunomodulatory potential of tiazofurin (TR) on experimental autoimmune encephalomyelitis (EAE) was investigated. Given continuously, TR dose-dependently suppressed the development of EAE in Dark Agouti (DA) rats immunized with either rat spinal cord homogenate (SCH) or myelin oligodendrocyte glycoprotein (MOG). Amelioration of clinical signs was also obtained when the drug was administered during the inductive phase only (day 0 to 8), or during the effector phase (day 10 to 20) of the disease. Efficacy of TR was further evaluated by adoptive transfer of the disease with myelin basic protein (MBP)-sensitized draining lymph node cells (DLNC). Cells from TR-protected rats failed to transfer the disease into naive syngeneic recipients; in addition, TR treatment of recipient rats that had received MBP-sensitized lymphoid cells diminished the adoptively transferred EAE. A reduction of clinical EAE in TR-treated rats was accompanied with the absence of mononuclear infiltration in the spinal cord and defective adhesive cell-cell interactions. The anti-MOG autoAb production was also decreased. Importantly, no evidence for a generalized impairment of the T cell activity, nor decreased in vitro proliferative antigen specific response of LNC from TR-treated animals was found. These results suggest that TR exerts its EAE protective and suppressive effects by limiting adhesive interactions involved in the autoimmune pathogenic process, and due to the lack of general immunosuppressive activity, it should be considered as a candidate drug for the treatment of neuroinflammatory diseases like multiple sclerosis (MS). (C) 2002 Elsevier Science B.V. All rights reserved.
T2  - Journal of Neuroimmunology
T1  - Down-regulation of experimental allergic encephalomyelitis in DA rats by tiazofurin
IS  - 1-2
VL  - 130
EP  - 77
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1788
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Savić-Radojević, Ana R and Maksimović-Ivanić, Danijela and Marković, Milos and Bumbaširević, Vesna D and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2002",
abstract = "The immunomodulatory potential of tiazofurin (TR) on experimental autoimmune encephalomyelitis (EAE) was investigated. Given continuously, TR dose-dependently suppressed the development of EAE in Dark Agouti (DA) rats immunized with either rat spinal cord homogenate (SCH) or myelin oligodendrocyte glycoprotein (MOG). Amelioration of clinical signs was also obtained when the drug was administered during the inductive phase only (day 0 to 8), or during the effector phase (day 10 to 20) of the disease. Efficacy of TR was further evaluated by adoptive transfer of the disease with myelin basic protein (MBP)-sensitized draining lymph node cells (DLNC). Cells from TR-protected rats failed to transfer the disease into naive syngeneic recipients; in addition, TR treatment of recipient rats that had received MBP-sensitized lymphoid cells diminished the adoptively transferred EAE. A reduction of clinical EAE in TR-treated rats was accompanied with the absence of mononuclear infiltration in the spinal cord and defective adhesive cell-cell interactions. The anti-MOG autoAb production was also decreased. Importantly, no evidence for a generalized impairment of the T cell activity, nor decreased in vitro proliferative antigen specific response of LNC from TR-treated animals was found. These results suggest that TR exerts its EAE protective and suppressive effects by limiting adhesive interactions involved in the autoimmune pathogenic process, and due to the lack of general immunosuppressive activity, it should be considered as a candidate drug for the treatment of neuroinflammatory diseases like multiple sclerosis (MS). (C) 2002 Elsevier Science B.V. All rights reserved.",
journal = "Journal of Neuroimmunology",
title = "Down-regulation of experimental allergic encephalomyelitis in DA rats by tiazofurin",
number = "1-2",
volume = "130",
pages = "77",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1788"
}

Stošić-Grujičić, S., Savić-Radojević, A. R., Maksimović-Ivanić, D., Marković, M., Bumbaširević, V. D., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2002). Down-regulation of experimental allergic encephalomyelitis in DA rats by tiazofurin. in Journal of Neuroimmunology, 130(1-2).
https://hdl.handle.net/21.15107/rcub_ibiss_1788

Stošić-Grujičić S, Savić-Radojević AR, Maksimović-Ivanić D, Marković M, Bumbaširević VD, Ramić ZD, Mostarica-Stojković MB. Down-regulation of experimental allergic encephalomyelitis in DA rats by tiazofurin. in Journal of Neuroimmunology. 2002;130(1-2):null-77.
https://hdl.handle.net/21.15107/rcub_ibiss_1788 .

Stošić-Grujičić, Stanislava, Savić-Radojević, Ana R, Maksimović-Ivanić, Danijela, Marković, Milos, Bumbaširević, Vesna D, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Down-regulation of experimental allergic encephalomyelitis in DA rats by tiazofurin" in Journal of Neuroimmunology, 130, no. 1-2 (2002),
https://hdl.handle.net/21.15107/rcub_ibiss_1788 .

TY  - JOUR
AU  - Trajković, Vladimir
AU  - Stošić-Grujičić, Stanislava
AU  - Samardzić, Tatjana
AU  - Marković, Miloš
AU  - Miljković, Đorđe
AU  - Ramić, Zorica
AU  - Mostarica Stojković, Marija
PY  - 2001
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5997
AB  - The effect of interleukin-17 (IL-17) on production of nitric oxide (NO) in rodent astrocytes was investigated. While IL-17 by itself did not induce NO production, it caused a dose-dependent enhancement of IFN-gamma-triggered NO synthesis in both mouse and rat primary astrocytes. In contrast, IL-17 was unable to stimulate NO synthesis in either murine or rat macrophages. IFN-gamma-triggered expression of mRNA for iNOS, but not for its transcription factor interferon regulatory factor-1 (IRF-1), was markedly elevated in IL-17-treated astrocytes. The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580. While IL-17 stimulated both IL-1beta and IL-6 production in astrocytes, only IL-1 was partly responsible for IL-17-induced NO release. Finally, IL-17 synergized with exogenous IL-1beta and TNF-alpha for astrocyte NO production. Having in mind a well-known neurotoxic action of NO, these results suggest a possible role for IL-17 in the inflammatory diseases of the CNS.
PB  - Amsterdam: Elsevier
T2  - Journal of Neuroimmunology
T1  - Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes
IS  - 2
VL  - 119
DO  - 10.1016/s0165-5728(01)00391-5
SP  - 183
EP  - 191
ER  - 

@article{
author = "Trajković, Vladimir and Stošić-Grujičić, Stanislava and Samardzić, Tatjana and Marković, Miloš and Miljković, Đorđe and Ramić, Zorica and Mostarica Stojković, Marija",
year = "2001",
abstract = "The effect of interleukin-17 (IL-17) on production of nitric oxide (NO) in rodent astrocytes was investigated. While IL-17 by itself did not induce NO production, it caused a dose-dependent enhancement of IFN-gamma-triggered NO synthesis in both mouse and rat primary astrocytes. In contrast, IL-17 was unable to stimulate NO synthesis in either murine or rat macrophages. IFN-gamma-triggered expression of mRNA for iNOS, but not for its transcription factor interferon regulatory factor-1 (IRF-1), was markedly elevated in IL-17-treated astrocytes. The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580. While IL-17 stimulated both IL-1beta and IL-6 production in astrocytes, only IL-1 was partly responsible for IL-17-induced NO release. Finally, IL-17 synergized with exogenous IL-1beta and TNF-alpha for astrocyte NO production. Having in mind a well-known neurotoxic action of NO, these results suggest a possible role for IL-17 in the inflammatory diseases of the CNS.",
publisher = "Amsterdam: Elsevier",
journal = "Journal of Neuroimmunology",
title = "Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes",
number = "2",
volume = "119",
doi = "10.1016/s0165-5728(01)00391-5",
pages = "183-191"
}

Trajković, V., Stošić-Grujičić, S., Samardzić, T., Marković, M., Miljković, Đ., Ramić, Z.,& Mostarica Stojković, M.. (2001). Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes. in Journal of Neuroimmunology
Amsterdam: Elsevier., 119(2), 183-191.
https://doi.org/10.1016/s0165-5728(01)00391-5

Trajković V, Stošić-Grujičić S, Samardzić T, Marković M, Miljković Đ, Ramić Z, Mostarica Stojković M. Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes. in Journal of Neuroimmunology. 2001;119(2):183-191.
doi:10.1016/s0165-5728(01)00391-5 .

Trajković, Vladimir, Stošić-Grujičić, Stanislava, Samardzić, Tatjana, Marković, Miloš, Miljković, Đorđe, Ramić, Zorica, Mostarica Stojković, Marija, "Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes" in Journal of Neuroimmunology, 119, no. 2 (2001):183-191,
https://doi.org/10.1016/s0165-5728(01)00391-5 . .