TY  - JOUR
AU  - Stevanović, Darko M
AU  - Starčević, Vesna P.
AU  - Vilimanović, Uros
AU  - Nesić, Dejan M
AU  - Vučićević, Ljubica
AU  - Misirkić Marjanović, Maja
AU  - Janjetović, Kristina
AU  - Savić, Emina
AU  - Popadić, Dusan M
AU  - Sudar, Emina M
AU  - Micić, Dragan D
AU  - Sumarac-Dumanović, Mirjana S
AU  - Trajković, Vladimir S
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1238
AB  - We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Brain Behavior and Immunity
T1  - Immunomodulatory actions of central ghrelin in diet-induced energy imbalance
IS  - 1
VL  - 26
EP  - 158
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1238
ER  - 

@article{
author = "Stevanović, Darko M and Starčević, Vesna P. and Vilimanović, Uros and Nesić, Dejan M and Vučićević, Ljubica and Misirkić Marjanović, Maja and Janjetović, Kristina and Savić, Emina and Popadić, Dusan M and Sudar, Emina M and Micić, Dragan D and Sumarac-Dumanović, Mirjana S and Trajković, Vladimir S",
year = "2012",
abstract = "We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Brain Behavior and Immunity",
title = "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance",
number = "1",
volume = "26",
pages = "158",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1238"
}

Stevanović, D. M., Starčević, V. P., Vilimanović, U., Nesić, D. M., Vučićević, L., Misirkić Marjanović, M., Janjetović, K., Savić, E., Popadić, D. M., Sudar, E. M., Micić, D. D., Sumarac-Dumanović, M. S.,& Trajković, V. S.. (2012). Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity, 26(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1238

Stevanović DM, Starčević VP, Vilimanović U, Nesić DM, Vučićević L, Misirkić Marjanović M, Janjetović K, Savić E, Popadić DM, Sudar EM, Micić DD, Sumarac-Dumanović MS, Trajković VS. Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity. 2012;26(1):null-158.
https://hdl.handle.net/21.15107/rcub_ibiss_1238 .

Stevanović, Darko M, Starčević, Vesna P., Vilimanović, Uros, Nesić, Dejan M, Vučićević, Ljubica, Misirkić Marjanović, Maja, Janjetović, Kristina, Savić, Emina, Popadić, Dusan M, Sudar, Emina M, Micić, Dragan D, Sumarac-Dumanović, Mirjana S, Trajković, Vladimir S, "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance" in Brain Behavior and Immunity, 26, no. 1 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1238 .

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  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
AU  - Maksimović-Ivanić, Danijela
AU  - Momčilović, Miljana
AU  - Popadić, Dušan
AU  - Harhaji-Trajković, Ljubica
AU  - Miljković, Đorđe
AU  - Metz, Christine
AU  - Mangano, Katia
AU  - Papaccio, Gianpacilo
AU  - Al-Abed, Yousef
AU  - Nicoletti, Ferdinando
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1528
AB  - Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine of the innate immune system that plays a major role in the induction of immunoinflammatory responses. To examine the role of endogenous MIF in the pathogenesis of type I diabetes (TID) we evaluated the effects of administration of neutralizing anti-MIF antibodies to NOD mice with accelerated forms of diabetes induced by injection of cyclophosphamide or by transfer of diabetogenic spleen cells. Both accelerated forms of diabetes were markedly reduced by anti-MIF antibody. Furthermore, MIF-deficient (MIF(-/-)) mice were less susceptible to the induction of immunoinflammatory diabetes, insulitis and apoptosis within the endocrine pancreas by multiple low doses of streptozotocin (MLD-STZ) than genetically matched wild type (WT) mice. MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1 beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1 beta, and iNOS in the islets of Langerhans. These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-1-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. These results suggest that MIF participates in T1D by controlling the functional activity of monocytes/macrophages and T cells and modulating their secretory capacity of pro- and anti-inflammatory molecules.
PB  - John Wiley and Sons
T2  - Journal of Cellular Physiology
T1  - Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus
IS  - 3
VL  - 215
DO  - 10.1002/jcp.21346
SP  - 665
EP  - 675
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1528
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Stojanović, Ivana D. and Maksimović-Ivanić, Danijela and Momčilović, Miljana and Popadić, Dušan and Harhaji-Trajković, Ljubica and Miljković, Đorđe and Metz, Christine and Mangano, Katia and Papaccio, Gianpacilo and Al-Abed, Yousef and Nicoletti, Ferdinando",
year = "2008",
abstract = "Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine of the innate immune system that plays a major role in the induction of immunoinflammatory responses. To examine the role of endogenous MIF in the pathogenesis of type I diabetes (TID) we evaluated the effects of administration of neutralizing anti-MIF antibodies to NOD mice with accelerated forms of diabetes induced by injection of cyclophosphamide or by transfer of diabetogenic spleen cells. Both accelerated forms of diabetes were markedly reduced by anti-MIF antibody. Furthermore, MIF-deficient (MIF(-/-)) mice were less susceptible to the induction of immunoinflammatory diabetes, insulitis and apoptosis within the endocrine pancreas by multiple low doses of streptozotocin (MLD-STZ) than genetically matched wild type (WT) mice. MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1 beta. Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1 beta, and iNOS in the islets of Langerhans. These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-1-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. These results suggest that MIF participates in T1D by controlling the functional activity of monocytes/macrophages and T cells and modulating their secretory capacity of pro- and anti-inflammatory molecules.",
publisher = "John Wiley and Sons",
journal = "Journal of Cellular Physiology",
title = "Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus",
number = "3",
volume = "215",
doi = "10.1002/jcp.21346",
pages = "665-675",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1528"
}

Stošić-Grujičić, S., Stojanović, I. D., Maksimović-Ivanić, D., Momčilović, M., Popadić, D., Harhaji-Trajković, L., Miljković, Đ., Metz, C., Mangano, K., Papaccio, G., Al-Abed, Y.,& Nicoletti, F.. (2008). Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. in Journal of Cellular Physiology
John Wiley and Sons., 215(3), 665-675.
https://doi.org/10.1002/jcp.21346
https://hdl.handle.net/21.15107/rcub_ibiss_1528

Stošić-Grujičić S, Stojanović ID, Maksimović-Ivanić D, Momčilović M, Popadić D, Harhaji-Trajković L, Miljković Đ, Metz C, Mangano K, Papaccio G, Al-Abed Y, Nicoletti F. Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus. in Journal of Cellular Physiology. 2008;215(3):665-675.
doi:10.1002/jcp.21346
https://hdl.handle.net/21.15107/rcub_ibiss_1528 .

Stošić-Grujičić, Stanislava, Stojanović, Ivana D., Maksimović-Ivanić, Danijela, Momčilović, Miljana, Popadić, Dušan, Harhaji-Trajković, Ljubica, Miljković, Đorđe, Metz, Christine, Mangano, Katia, Papaccio, Gianpacilo, Al-Abed, Yousef, Nicoletti, Ferdinando, "Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus" in Journal of Cellular Physiology, 215, no. 3 (2008):665-675,
https://doi.org/10.1002/jcp.21346 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1528 .

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  - Momčilović, Miljana
AU  - Miljković, Zeljka
AU  - Popadić, Dusan M
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1497
AB  - Interferon-gamma (IFN-gamma) and interleukin-17 (IL-17) have been involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE). We have carried out a follow-up study of the expression and production of these cytokines, as well as of cells expressing these cytokines during the course of active EAE in Dark Agouti (DA) rats. As a result, IL-17, but not IFN-gamma expression and production had the peak value in draining lymph nodes (DLN) during the induction phase of the disease, and in spinal cords (SC) at the onset of clinical signs of the disease, and then declined toward the resolution of the disease. Also, a significant proportion of IFN-gamma/IL-17 double-positive cells was observed in SC of DA rats in active EAE. Importantly, the highest proportion of IL-17 single positive and double-positive cells, but not of IFN-gamma single positive cells, was observed at the onset of the disease. The observed difference in the kinetics of IFN-gamma and IL-17 expression during active EAE in DA rats suggests different roles these cytokines might have in the pathogenesis of the disease. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
T2  - Neuroscience Letters
T1  - Kinetics of IFN-gamma and IL-17 expression and production in active experimental autoimmune encephalomyelitis in Dark Agouti rats
IS  - 2-3
VL  - 447
EP  - 152
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1497
ER  - 

@article{
author = "Momčilović, Miljana and Miljković, Zeljka and Popadić, Dusan M and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2008",
abstract = "Interferon-gamma (IFN-gamma) and interleukin-17 (IL-17) have been involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE). We have carried out a follow-up study of the expression and production of these cytokines, as well as of cells expressing these cytokines during the course of active EAE in Dark Agouti (DA) rats. As a result, IL-17, but not IFN-gamma expression and production had the peak value in draining lymph nodes (DLN) during the induction phase of the disease, and in spinal cords (SC) at the onset of clinical signs of the disease, and then declined toward the resolution of the disease. Also, a significant proportion of IFN-gamma/IL-17 double-positive cells was observed in SC of DA rats in active EAE. Importantly, the highest proportion of IL-17 single positive and double-positive cells, but not of IFN-gamma single positive cells, was observed at the onset of the disease. The observed difference in the kinetics of IFN-gamma and IL-17 expression during active EAE in DA rats suggests different roles these cytokines might have in the pathogenesis of the disease. (C) 2008 Elsevier Ireland Ltd. All rights reserved.",
journal = "Neuroscience Letters",
title = "Kinetics of IFN-gamma and IL-17 expression and production in active experimental autoimmune encephalomyelitis in Dark Agouti rats",
number = "2-3",
volume = "447",
pages = "152",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1497"
}

Momčilović, M., Miljković, Z., Popadić, D. M., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2008). Kinetics of IFN-gamma and IL-17 expression and production in active experimental autoimmune encephalomyelitis in Dark Agouti rats. in Neuroscience Letters, 447(2-3).
https://hdl.handle.net/21.15107/rcub_ibiss_1497

Momčilović M, Miljković Z, Popadić DM, Miljković Đ, Mostarica-Stojković MB. Kinetics of IFN-gamma and IL-17 expression and production in active experimental autoimmune encephalomyelitis in Dark Agouti rats. in Neuroscience Letters. 2008;447(2-3):null-152.
https://hdl.handle.net/21.15107/rcub_ibiss_1497 .

Momčilović, Miljana, Miljković, Zeljka, Popadić, Dusan M, Miljković, Đorđe, Mostarica-Stojković, Marija B, "Kinetics of IFN-gamma and IL-17 expression and production in active experimental autoimmune encephalomyelitis in Dark Agouti rats" in Neuroscience Letters, 447, no. 2-3 (2008),
https://hdl.handle.net/21.15107/rcub_ibiss_1497 .

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  - 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  - JOUR
AU  - Samardžić, Tatjana S.
AU  - Janković, V
AU  - Stošić-Grujičić, Stanislava
AU  - Popadić, Dusan M
AU  - Trajković, Vladimir S
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1815
AB  - The effect of phosphodiesterase-inhibiting anti-inflammatory drug pentoxifylline (PTX) on LPS-induced IL-18 synthesis and IL-18-mediated IFN-gamma -induction were investigated. In a dose-dependent manner PTX inhibited production of IL-18 in LPS-treated cultures of murine spleen cells and bone marrow-derived macrophages. Similarly, PTX treatment significantly reduced blood IL-18 levels and expression of spleen IL-18 mRNA in LPS-challenged mice. The inhibitory effect of PTX was specific for IL-18, since LPS-induced IL-12 p40 release was not suppressed either in splenocyte cultures or blood of LPS-injected animals. Synergistic induction of IFN-gamma by combined IL-12/IL-18 treatment was also inhibited by PTX in vitro and in vivo. Experiments with IL-12 pretreatment of splenocytes, followed by IL-18 stimulation, revealed that PTX suppressed both IL-12 and IL-18 signals responsible for IFN-gamma induction. These results suggest that interference with IL-18 synthesis and IFN-gamma -inducing activity might contribute to anti-inflammatory actions of PTX.
T2  - Clinical and Experimental Immunology
T1  - Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18
IS  - 2
VL  - 124
EP  - 281
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1815
ER  - 

@article{
author = "Samardžić, Tatjana S. and Janković, V and Stošić-Grujičić, Stanislava and Popadić, Dusan M and Trajković, Vladimir S",
year = "2001",
abstract = "The effect of phosphodiesterase-inhibiting anti-inflammatory drug pentoxifylline (PTX) on LPS-induced IL-18 synthesis and IL-18-mediated IFN-gamma -induction were investigated. In a dose-dependent manner PTX inhibited production of IL-18 in LPS-treated cultures of murine spleen cells and bone marrow-derived macrophages. Similarly, PTX treatment significantly reduced blood IL-18 levels and expression of spleen IL-18 mRNA in LPS-challenged mice. The inhibitory effect of PTX was specific for IL-18, since LPS-induced IL-12 p40 release was not suppressed either in splenocyte cultures or blood of LPS-injected animals. Synergistic induction of IFN-gamma by combined IL-12/IL-18 treatment was also inhibited by PTX in vitro and in vivo. Experiments with IL-12 pretreatment of splenocytes, followed by IL-18 stimulation, revealed that PTX suppressed both IL-12 and IL-18 signals responsible for IFN-gamma induction. These results suggest that interference with IL-18 synthesis and IFN-gamma -inducing activity might contribute to anti-inflammatory actions of PTX.",
journal = "Clinical and Experimental Immunology",
title = "Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18",
number = "2",
volume = "124",
pages = "281",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1815"
}

Samardžić, T. S., Janković, V., Stošić-Grujičić, S., Popadić, D. M.,& Trajković, V. S.. (2001). Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18. in Clinical and Experimental Immunology, 124(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1815

Samardžić TS, Janković V, Stošić-Grujičić S, Popadić DM, Trajković VS. Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18. in Clinical and Experimental Immunology. 2001;124(2):null-281.
https://hdl.handle.net/21.15107/rcub_ibiss_1815 .

Samardžić, Tatjana S., Janković, V, Stošić-Grujičić, Stanislava, Popadić, Dusan M, Trajković, Vladimir S, "Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18" in Clinical and Experimental Immunology, 124, no. 2 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1815 .

TY  - JOUR
AU  - Janković, V
AU  - Samardžić, Tatjana S.
AU  - Stošić-Grujičić, Stanislava
AU  - Popadić, Dusan M
AU  - Trajković, Vladimir S
PY  - 2000
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1834
AB  - The influence of a novel immunomodulating drug, leflunomide, on iNOS-dependent nitric oxide (NO) production in rodent macrophages and fibroblasts was investigated. Leflunomide's active metabolite A77 1726 caused a dose-dependent decrease of NO production in IFN-gamma-treated L929 fibroblasts. The observed effect was cell-specific, as well as stimulus-specific, since A77 1726 did not affect NO production in IFN-gamma-stimulated murine peritoneal macrophages or db-cAMP-treated L929 cells. A77 1726 reduced expression of IFN-gamma-induced iNOS and IRF-1 mRNA in L929 cells, while iNOS enzymatic activity remained unchanged. Specific inhibitor of MAP kinase kinase (MEK), PD98059, but not unselective protein kinase inhibitor genistein, completely mimicked cell-type-specific and stimulus-specific NO-inhibitory action of leflunomide. Therefore, the recently described inhibition of MEK/MAP pathway by leflunomide could present a possible mechanism for its suppression of iNOS activation in L929 fibroblasts. Finally, a similar inhibitory effect of A77 1726 on both NO production and iNOS mRNA expression was observed also in IFN-gamma + LPS-activated murine and rat primary fibroblasts. (C) 2000 Academic Press.
T2  - Cellular Immunology
T1  - Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide
IS  - 2
VL  - 199
EP  - 80
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1834
ER  - 

@article{
author = "Janković, V and Samardžić, Tatjana S. and Stošić-Grujičić, Stanislava and Popadić, Dusan M and Trajković, Vladimir S",
year = "2000",
abstract = "The influence of a novel immunomodulating drug, leflunomide, on iNOS-dependent nitric oxide (NO) production in rodent macrophages and fibroblasts was investigated. Leflunomide's active metabolite A77 1726 caused a dose-dependent decrease of NO production in IFN-gamma-treated L929 fibroblasts. The observed effect was cell-specific, as well as stimulus-specific, since A77 1726 did not affect NO production in IFN-gamma-stimulated murine peritoneal macrophages or db-cAMP-treated L929 cells. A77 1726 reduced expression of IFN-gamma-induced iNOS and IRF-1 mRNA in L929 cells, while iNOS enzymatic activity remained unchanged. Specific inhibitor of MAP kinase kinase (MEK), PD98059, but not unselective protein kinase inhibitor genistein, completely mimicked cell-type-specific and stimulus-specific NO-inhibitory action of leflunomide. Therefore, the recently described inhibition of MEK/MAP pathway by leflunomide could present a possible mechanism for its suppression of iNOS activation in L929 fibroblasts. Finally, a similar inhibitory effect of A77 1726 on both NO production and iNOS mRNA expression was observed also in IFN-gamma + LPS-activated murine and rat primary fibroblasts. (C) 2000 Academic Press.",
journal = "Cellular Immunology",
title = "Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide",
number = "2",
volume = "199",
pages = "80",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1834"
}

Janković, V., Samardžić, T. S., Stošić-Grujičić, S., Popadić, D. M.,& Trajković, V. S.. (2000). Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide. in Cellular Immunology, 199(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1834

Janković V, Samardžić TS, Stošić-Grujičić S, Popadić DM, Trajković VS. Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide. in Cellular Immunology. 2000;199(2):null-80.
https://hdl.handle.net/21.15107/rcub_ibiss_1834 .

Janković, V, Samardžić, Tatjana S., Stošić-Grujičić, Stanislava, Popadić, Dusan M, Trajković, Vladimir S, "Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide" in Cellular Immunology, 199, no. 2 (2000),
https://hdl.handle.net/21.15107/rcub_ibiss_1834 .