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  - 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  - Marković, Milos
AU  - Knežević, Nikola Z
AU  - Momčilović, Miljana
AU  - Grgurić-Sipka, Sanja R
AU  - Harhaji-Trajković, Ljubica
AU  - Trajković, Vladimir S
AU  - Mostarica-Stojković, Marija B
AU  - Sabo, Tibor J
AU  - Miljković, Đorđe
PY  - 2005
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1696
AB  - There has been a continuing effort for the discovery of novel platinum(IV)-based antitumor compounds with better therapeutic performances than cisplatin. In the present work, the anticancer action of recently synthesized Pt(IV)-based complex [Pt(HPxSC)Cl-3] was investigated using rat and human astrocytoma cell lines C6 and U251. [Pt(HPxSC)Cl-3] markedly reduced the number of cultured astrocytoma Cells (IC50, 80 mu M), as determined by crystal violet assay. The Pt(IV) complex induced apoptotic death of tumor cells, as flow cytometry analysis of the propidium iodide-stained cellular DNA revealed approx. 30% of hypodiploid cells in [Pt(HPxSC)Cl-3]-treated astrocytoma cell cultures. On the other hand, [Pt(HPxSC)Cl-3] at 200 mu M did not affect the viability of rat primary astrocytes, unlike the established anticancer drug cisplatin, which displayed high toxicity toward both astrocytoma cells (IC50, 15 mu M) and primary astrocytes (IC50, 20 mu M). Moreover, [Pt(HPxSC)Cl-3] at 100 mu M did not interfere with the ability of rat peritoneal macrophages to produce important antitumor molecules nitric oxide and tumor necrosis factor-a. Finally, we assessed the ability of [Pt(HPxSC)Cl-3] to restrain growth of some bacterial and yeast strains, but it showed rather limited antimicrobial activity. (c) 2005 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - [Pt(HPxSC)Cl-3], a novel platinum(IV) compound with anticancer properties
IS  - 1-2
VL  - 517
EP  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1696
ER  - 

@article{
author = "Marković, Milos and Knežević, Nikola Z and Momčilović, Miljana and Grgurić-Sipka, Sanja R and Harhaji-Trajković, Ljubica and Trajković, Vladimir S and Mostarica-Stojković, Marija B and Sabo, Tibor J and Miljković, Đorđe",
year = "2005",
abstract = "There has been a continuing effort for the discovery of novel platinum(IV)-based antitumor compounds with better therapeutic performances than cisplatin. In the present work, the anticancer action of recently synthesized Pt(IV)-based complex [Pt(HPxSC)Cl-3] was investigated using rat and human astrocytoma cell lines C6 and U251. [Pt(HPxSC)Cl-3] markedly reduced the number of cultured astrocytoma Cells (IC50, 80 mu M), as determined by crystal violet assay. The Pt(IV) complex induced apoptotic death of tumor cells, as flow cytometry analysis of the propidium iodide-stained cellular DNA revealed approx. 30% of hypodiploid cells in [Pt(HPxSC)Cl-3]-treated astrocytoma cell cultures. On the other hand, [Pt(HPxSC)Cl-3] at 200 mu M did not affect the viability of rat primary astrocytes, unlike the established anticancer drug cisplatin, which displayed high toxicity toward both astrocytoma cells (IC50, 15 mu M) and primary astrocytes (IC50, 20 mu M). Moreover, [Pt(HPxSC)Cl-3] at 100 mu M did not interfere with the ability of rat peritoneal macrophages to produce important antitumor molecules nitric oxide and tumor necrosis factor-a. Finally, we assessed the ability of [Pt(HPxSC)Cl-3] to restrain growth of some bacterial and yeast strains, but it showed rather limited antimicrobial activity. (c) 2005 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "[Pt(HPxSC)Cl-3], a novel platinum(IV) compound with anticancer properties",
number = "1-2",
volume = "517",
pages = "34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1696"
}

Marković, M., Knežević, N. Z., Momčilović, M., Grgurić-Sipka, S. R., Harhaji-Trajković, L., Trajković, V. S., Mostarica-Stojković, M. B., Sabo, T. J.,& Miljković, Đ.. (2005). [Pt(HPxSC)Cl-3], a novel platinum(IV) compound with anticancer properties. in European Journal of Pharmacology, 517(1-2).
https://hdl.handle.net/21.15107/rcub_ibiss_1696

Marković M, Knežević NZ, Momčilović M, Grgurić-Sipka SR, Harhaji-Trajković L, Trajković VS, Mostarica-Stojković MB, Sabo TJ, Miljković Đ. [Pt(HPxSC)Cl-3], a novel platinum(IV) compound with anticancer properties. in European Journal of Pharmacology. 2005;517(1-2):null-34.
https://hdl.handle.net/21.15107/rcub_ibiss_1696 .

Marković, Milos, Knežević, Nikola Z, Momčilović, Miljana, Grgurić-Sipka, Sanja R, Harhaji-Trajković, Ljubica, Trajković, Vladimir S, Mostarica-Stojković, Marija B, Sabo, Tibor J, Miljković, Đorđe, "[Pt(HPxSC)Cl-3], a novel platinum(IV) compound with anticancer properties" in European Journal of Pharmacology, 517, no. 1-2 (2005),
https://hdl.handle.net/21.15107/rcub_ibiss_1696 .

TY  - CONF
AU  - Marković, Milos
AU  - Miljković, Đorđe
AU  - Trajković, Vladimir S
AU  - Mostarica-Stojković, Marija B
AU  - Stošić-Grujičić, Stanislava
PY  - 2005
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1695
C3  - Inflammation Research
T1  - Prevention of experimental autoimmune diabetes with complete Freund's adjuvant in mice - role of nitric oxide
IS  - null
VL  - 54
EP  - S132
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1695
ER  - 

@conference{
author = "Marković, Milos and Miljković, Đorđe and Trajković, Vladimir S and Mostarica-Stojković, Marija B and Stošić-Grujičić, Stanislava",
year = "2005",
journal = "Inflammation Research",
title = "Prevention of experimental autoimmune diabetes with complete Freund's adjuvant in mice - role of nitric oxide",
number = "null",
volume = "54",
pages = "S132",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1695"
}

Marković, M., Miljković, Đ., Trajković, V. S., Mostarica-Stojković, M. B.,& Stošić-Grujičić, S.. (2005). Prevention of experimental autoimmune diabetes with complete Freund's adjuvant in mice - role of nitric oxide. in Inflammation Research, 54(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1695

Marković M, Miljković Đ, Trajković VS, Mostarica-Stojković MB, Stošić-Grujičić S. Prevention of experimental autoimmune diabetes with complete Freund's adjuvant in mice - role of nitric oxide. in Inflammation Research. 2005;54(null):null-S132.
https://hdl.handle.net/21.15107/rcub_ibiss_1695 .

Marković, Milos, Miljković, Đorđe, Trajković, Vladimir S, Mostarica-Stojković, Marija B, Stošić-Grujičić, Stanislava, "Prevention of experimental autoimmune diabetes with complete Freund's adjuvant in mice - role of nitric oxide" in Inflammation Research, 54, no. null (2005),
https://hdl.handle.net/21.15107/rcub_ibiss_1695 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Stojanović, Ivana D.
AU  - Sajić, Marija
AU  - Vucković, Olivera
AU  - Harhaji-Trajković, Ljubica
AU  - Marković, Milos
AU  - Trajković, Vladimir S
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1741
AB  - Given the important role of gaseous free radical nitric oxide (NO) in tumor cell biology, we investigated the ability of the anti-cancer drugs 5-Aza-2'-deoxycytidine (ADC) and paclitaxel to modulate NO production in mouse L929 fibrosarcoma cells. Both drugs reduced IFN-gamma-stimulated NO release in cultures of L929 and primary fibroblasts, but not in mouse peritoneal macrophages. The inhibitory effect was due to the reduced expression of inducible NO synthase (iNOS), the enzyme responsible for cytokine-induced intracellular NO synthesis, as both agents markedly suppressed the interferon-ganuna (IFN-gamma)-triggered increase in iNOS concentration in L929 cells. In addition, ADC and paclitaxel prevented the FFN-gamma-triggered activation of p44/p42 mitogen-activated protein (MAP) kinase in L929 fibroblasts, suggesting a possible mechanism for the observed inhibition of iNOS expression. These results might have important implications for the therapeutic effect of ADC and paclitaxel, since their inhibitory action on NO release partly neutralized the NO-dependent toxicity of IFN-gamma on L929 fibrosarcoma cells. (C) 2003 Elsevier B.V All rights reserved.
T2  - European Journal of Pharmacology
T1  - 5-Aza-2 '-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells
IS  - 1-3
VL  - 485
DO  - 10.1016/j.ejphar.2003.11.057
SP  - 81
EP  - 88
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1741
ER  - 

@article{
author = "Miljković, Đorđe and Stojanović, Ivana D. and Sajić, Marija and Vucković, Olivera and Harhaji-Trajković, Ljubica and Marković, Milos and Trajković, Vladimir S",
year = "2004",
abstract = "Given the important role of gaseous free radical nitric oxide (NO) in tumor cell biology, we investigated the ability of the anti-cancer drugs 5-Aza-2'-deoxycytidine (ADC) and paclitaxel to modulate NO production in mouse L929 fibrosarcoma cells. Both drugs reduced IFN-gamma-stimulated NO release in cultures of L929 and primary fibroblasts, but not in mouse peritoneal macrophages. The inhibitory effect was due to the reduced expression of inducible NO synthase (iNOS), the enzyme responsible for cytokine-induced intracellular NO synthesis, as both agents markedly suppressed the interferon-ganuna (IFN-gamma)-triggered increase in iNOS concentration in L929 cells. In addition, ADC and paclitaxel prevented the FFN-gamma-triggered activation of p44/p42 mitogen-activated protein (MAP) kinase in L929 fibroblasts, suggesting a possible mechanism for the observed inhibition of iNOS expression. These results might have important implications for the therapeutic effect of ADC and paclitaxel, since their inhibitory action on NO release partly neutralized the NO-dependent toxicity of IFN-gamma on L929 fibrosarcoma cells. (C) 2003 Elsevier B.V All rights reserved.",
journal = "European Journal of Pharmacology",
title = "5-Aza-2 '-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells",
number = "1-3",
volume = "485",
doi = "10.1016/j.ejphar.2003.11.057",
pages = "81-88",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1741"
}

Miljković, Đ., Stojanović, I. D., Sajić, M., Vucković, O., Harhaji-Trajković, L., Marković, M.,& Trajković, V. S.. (2004). 5-Aza-2 '-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells. in European Journal of Pharmacology, 485(1-3), 81-88.
https://doi.org/10.1016/j.ejphar.2003.11.057
https://hdl.handle.net/21.15107/rcub_ibiss_1741

Miljković Đ, Stojanović ID, Sajić M, Vucković O, Harhaji-Trajković L, Marković M, Trajković VS. 5-Aza-2 '-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells. in European Journal of Pharmacology. 2004;485(1-3):81-88.
doi:10.1016/j.ejphar.2003.11.057
https://hdl.handle.net/21.15107/rcub_ibiss_1741 .

Miljković, Đorđe, Stojanović, Ivana D., Sajić, Marija, Vucković, Olivera, Harhaji-Trajković, Ljubica, Marković, Milos, Trajković, Vladimir S, "5-Aza-2 '-deoxycytidine and paclitaxel inhibit inducible nitric oxide synthase activation in fibrosarcoma cells" in European Journal of Pharmacology, 485, no. 1-3 (2004):81-88,
https://doi.org/10.1016/j.ejphar.2003.11.057 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1741 .

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  - Miljković, Đorđe
AU  - Marković, Miloš
AU  - Bogdanović, Natalija
AU  - Mostarica-Stojković, Marija
AU  - Trajković, Vladimir
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1800
AB  - Nitric oxide (NO) is a highly reactive free radical with profound tumoricidal activity, produced by both macrophages and tumor cells. While it has been postulated that necrotic tumor cells can augment macrophage anti-tumor action, we investigated the effect of tumor cell necrosis on NO synthesis and viability of L929 fibrosarcoma and C6 astrocytoma cell lines. The presence of necrotic tumor cells dose-dependently reduced NO production in IFN-gamma stimulated L929 cells, and rescued them from NO-dependent autotoxicity. This effect was mediated through soluble products, since it was completely preserved after blocking the contact between the necrotic and live cells. On the other hand, apoptotic tumor cells were unable to suppress IFN-gamma-triggered NO release and subsequent decrease of cell respiration in L929 cultures. Similar results were obtained with C6 astrocytoma cell line. This down-regulation of NO synthesis in response to necrotic cell products was not specific for tumor cell lines, since necrotic tumor cells markedly suppressed NO production in cytokine-stimulated primary fibroblasts and astrocytes. In contrast, both murine and rat peritoneal macrophages readily increased their basal or IFN-gamma-induced NO production when incubated with necrotic tumor cells. Taken together, these results suggest that tumor cell necrosis might promote or restrict tumor growth through suppression or enhancement of NO synthesis in tumor cells and macrophages, respectively, with net effect presumably depending on the extent of macrophage infiltration. (C) 2002 Elsevier Science (USA). All rights reserved.
PB  - Elsevier
T2  - Cellular Immunology
T1  - Necrotic tumor cells oppositely affect nitric oxide production in tumor cell lines and macrophages
IS  - 1
VL  - 215
DO  - 10.1016/S0008-8749(02)00008-4
SP  - 72
EP  - 77
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1800
ER  - 

@article{
author = "Miljković, Đorđe and Marković, Miloš and Bogdanović, Natalija and Mostarica-Stojković, Marija and Trajković, Vladimir",
year = "2002",
abstract = "Nitric oxide (NO) is a highly reactive free radical with profound tumoricidal activity, produced by both macrophages and tumor cells. While it has been postulated that necrotic tumor cells can augment macrophage anti-tumor action, we investigated the effect of tumor cell necrosis on NO synthesis and viability of L929 fibrosarcoma and C6 astrocytoma cell lines. The presence of necrotic tumor cells dose-dependently reduced NO production in IFN-gamma stimulated L929 cells, and rescued them from NO-dependent autotoxicity. This effect was mediated through soluble products, since it was completely preserved after blocking the contact between the necrotic and live cells. On the other hand, apoptotic tumor cells were unable to suppress IFN-gamma-triggered NO release and subsequent decrease of cell respiration in L929 cultures. Similar results were obtained with C6 astrocytoma cell line. This down-regulation of NO synthesis in response to necrotic cell products was not specific for tumor cell lines, since necrotic tumor cells markedly suppressed NO production in cytokine-stimulated primary fibroblasts and astrocytes. In contrast, both murine and rat peritoneal macrophages readily increased their basal or IFN-gamma-induced NO production when incubated with necrotic tumor cells. Taken together, these results suggest that tumor cell necrosis might promote or restrict tumor growth through suppression or enhancement of NO synthesis in tumor cells and macrophages, respectively, with net effect presumably depending on the extent of macrophage infiltration. (C) 2002 Elsevier Science (USA). All rights reserved.",
publisher = "Elsevier",
journal = "Cellular Immunology",
title = "Necrotic tumor cells oppositely affect nitric oxide production in tumor cell lines and macrophages",
number = "1",
volume = "215",
doi = "10.1016/S0008-8749(02)00008-4",
pages = "72-77",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1800"
}

Miljković, Đ., Marković, M., Bogdanović, N., Mostarica-Stojković, M.,& Trajković, V.. (2002). Necrotic tumor cells oppositely affect nitric oxide production in tumor cell lines and macrophages. in Cellular Immunology
Elsevier., 215(1), 72-77.
https://doi.org/10.1016/S0008-8749(02)00008-4
https://hdl.handle.net/21.15107/rcub_ibiss_1800

Miljković Đ, Marković M, Bogdanović N, Mostarica-Stojković M, Trajković V. Necrotic tumor cells oppositely affect nitric oxide production in tumor cell lines and macrophages. in Cellular Immunology. 2002;215(1):72-77.
doi:10.1016/S0008-8749(02)00008-4
https://hdl.handle.net/21.15107/rcub_ibiss_1800 .

Miljković, Đorđe, Marković, Miloš, Bogdanović, Natalija, Mostarica-Stojković, Marija, Trajković, Vladimir, "Necrotic tumor cells oppositely affect nitric oxide production in tumor cell lines and macrophages" in Cellular Immunology, 215, no. 1 (2002):72-77,
https://doi.org/10.1016/S0008-8749(02)00008-4 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1800 .

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 .