TY  - JOUR
AU  - Trajković, Vladimir
AU  - Janković, Vladimir
AU  - Badovinac, Vladimir
AU  - Samardžić, Tamara
AU  - Maksimović-Ivanić, Danijela
AU  - Popadić, Dušan
PY  - 1999
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3823
AB  - The effects of immunosuppressant cyclosporin A (CsA) on nitric oxide (NO) production and inducible NO synthase (iNOS) activity in murine L929 fibroblasts were investigated. IFN-gamma-induced NO production in L929 cells was mediated through an iNOS-dependent L-arginine-NO pathway, since it was abrogated by a selective inhibitor of iNOS, aminoguanidine. CsA applied simultaneously with IFN-gamma caused a dose-dependent reduction of NO synthesis in L929 cells. However, CsA did not influence the enzymatic activity of iNOS, since it failed to affect NO production in cells in which iNOS had already been induced with IFN-gamma and any further induction was blocked by the protein-synthesis inhibitor cycloheximide. IFN-gamma-triggered expression of mRNA for interferon regulatory factor-1 was not reduced by CsA-treatment, suggesting that this iNOS transcription factor is not a target in CsA-mediated inhibition of NO synthesis. Finally, FK506 was not able to mimic the inhibitory effect of CsA on NO production in L929 cells, indicating the calcineurin-independent mechanism of CsA action. These results indicate that CsA suppresses NO synthesis in L929 cells independent of calcineurin inhibition, and interfering with intracellular pathways involved in the iNOS induction, rather than inhibiting its enzymatic activity.
PB  - New Jerswy: Wiley-VCH Verlag GmbH & Co
T2  - Scandinavian Journal of Immunology
T1  - Cyclosporin A suppresses the induction of nitric oxide synthesis in interferon-gamma-treated L929 fibroblasts
IS  - 2
VL  - 49
DO  - 10.1046/j.1365-3083.1999.00468.x
SP  - 126
EP  - 130
ER  - 

@article{
author = "Trajković, Vladimir and Janković, Vladimir and Badovinac, Vladimir and Samardžić, Tamara and Maksimović-Ivanić, Danijela and Popadić, Dušan",
year = "1999",
abstract = "The effects of immunosuppressant cyclosporin A (CsA) on nitric oxide (NO) production and inducible NO synthase (iNOS) activity in murine L929 fibroblasts were investigated. IFN-gamma-induced NO production in L929 cells was mediated through an iNOS-dependent L-arginine-NO pathway, since it was abrogated by a selective inhibitor of iNOS, aminoguanidine. CsA applied simultaneously with IFN-gamma caused a dose-dependent reduction of NO synthesis in L929 cells. However, CsA did not influence the enzymatic activity of iNOS, since it failed to affect NO production in cells in which iNOS had already been induced with IFN-gamma and any further induction was blocked by the protein-synthesis inhibitor cycloheximide. IFN-gamma-triggered expression of mRNA for interferon regulatory factor-1 was not reduced by CsA-treatment, suggesting that this iNOS transcription factor is not a target in CsA-mediated inhibition of NO synthesis. Finally, FK506 was not able to mimic the inhibitory effect of CsA on NO production in L929 cells, indicating the calcineurin-independent mechanism of CsA action. These results indicate that CsA suppresses NO synthesis in L929 cells independent of calcineurin inhibition, and interfering with intracellular pathways involved in the iNOS induction, rather than inhibiting its enzymatic activity.",
publisher = "New Jerswy: Wiley-VCH Verlag GmbH & Co",
journal = "Scandinavian Journal of Immunology",
title = "Cyclosporin A suppresses the induction of nitric oxide synthesis in interferon-gamma-treated L929 fibroblasts",
number = "2",
volume = "49",
doi = "10.1046/j.1365-3083.1999.00468.x",
pages = "126-130"
}

Trajković, V., Janković, V., Badovinac, V., Samardžić, T., Maksimović-Ivanić, D.,& Popadić, D.. (1999). Cyclosporin A suppresses the induction of nitric oxide synthesis in interferon-gamma-treated L929 fibroblasts. in Scandinavian Journal of Immunology
New Jerswy: Wiley-VCH Verlag GmbH & Co., 49(2), 126-130.
https://doi.org/10.1046/j.1365-3083.1999.00468.x

Trajković V, Janković V, Badovinac V, Samardžić T, Maksimović-Ivanić D, Popadić D. Cyclosporin A suppresses the induction of nitric oxide synthesis in interferon-gamma-treated L929 fibroblasts. in Scandinavian Journal of Immunology. 1999;49(2):126-130.
doi:10.1046/j.1365-3083.1999.00468.x .

Trajković, Vladimir, Janković, Vladimir, Badovinac, Vladimir, Samardžić, Tamara, Maksimović-Ivanić, Danijela, Popadić, Dušan, "Cyclosporin A suppresses the induction of nitric oxide synthesis in interferon-gamma-treated L929 fibroblasts" in Scandinavian Journal of Immunology, 49, no. 2 (1999):126-130,
https://doi.org/10.1046/j.1365-3083.1999.00468.x . .

TY  - JOUR
AU  - Badovinac, V
AU  - Mostarica-Stojković, Marija B
AU  - Dinarello, CA
AU  - Stošić-Grujičić, Stanislava
PY  - 1998
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1860
AB  - Considering the role of pleiotropic interleukin-1 (IL-1) in inflammation and autoimmunity, studies were designed to examine whether specific blockade of IL-1 may influence these processes in the CNS. Although the role of CD4(+) T cells in eliciting clinical signs of experimental autoimmune encephalomyelitis (EAE) has been unequivocally demonstrated, the exact mechanism by which encephalitogenic cells initiate disease process and bring about clinical signs still remains to be defined. We have evaluated the effect of human recombinant interleukin-1 receptor antagonist (IL-1Ra) in vivo on the course of actively induced EAE in highly susceptible Dark Agouti (DA) rats. The rats which were treated during the induction phase of disease (days 0-6) with IL-1Ra (350 mu g/rat/day) developed milder signs of EAE, when compared to saline-treated control animals immunized with encephalitogen, which developed severe single episode disease. The transfer of lymph node cells (LNC) isolated from MBP-primed DA rats and stimulated in vitro with MBP and ConA to naive syngeneic animals resulted in the development of EAE in all recipients. However, rats injected with LNC that have been stimulated in vitro in the presence of IL-1Ra (10 mu g/ml) developed significantly milder disease. Diminished encephalitogenic capacity of LNC correlated with lower proliferative response to antigen and mitogen and decreased expression of IL-2 receptors. These data provide further evidence that IL-1 is an important factor for activation of EAE inducing T lymphocytes. (C) 1998 Elsevier Science B.V. All rights reserved.
T2  - Journal of Neuroimmunology
T1  - Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells
IS  - 1
VL  - 85
EP  - 95
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1860
ER  - 

@article{
author = "Badovinac, V and Mostarica-Stojković, Marija B and Dinarello, CA and Stošić-Grujičić, Stanislava",
year = "1998",
abstract = "Considering the role of pleiotropic interleukin-1 (IL-1) in inflammation and autoimmunity, studies were designed to examine whether specific blockade of IL-1 may influence these processes in the CNS. Although the role of CD4(+) T cells in eliciting clinical signs of experimental autoimmune encephalomyelitis (EAE) has been unequivocally demonstrated, the exact mechanism by which encephalitogenic cells initiate disease process and bring about clinical signs still remains to be defined. We have evaluated the effect of human recombinant interleukin-1 receptor antagonist (IL-1Ra) in vivo on the course of actively induced EAE in highly susceptible Dark Agouti (DA) rats. The rats which were treated during the induction phase of disease (days 0-6) with IL-1Ra (350 mu g/rat/day) developed milder signs of EAE, when compared to saline-treated control animals immunized with encephalitogen, which developed severe single episode disease. The transfer of lymph node cells (LNC) isolated from MBP-primed DA rats and stimulated in vitro with MBP and ConA to naive syngeneic animals resulted in the development of EAE in all recipients. However, rats injected with LNC that have been stimulated in vitro in the presence of IL-1Ra (10 mu g/ml) developed significantly milder disease. Diminished encephalitogenic capacity of LNC correlated with lower proliferative response to antigen and mitogen and decreased expression of IL-2 receptors. These data provide further evidence that IL-1 is an important factor for activation of EAE inducing T lymphocytes. (C) 1998 Elsevier Science B.V. All rights reserved.",
journal = "Journal of Neuroimmunology",
title = "Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells",
number = "1",
volume = "85",
pages = "95",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1860"
}

Badovinac, V., Mostarica-Stojković, M. B., Dinarello, C.,& Stošić-Grujičić, S.. (1998). Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells. in Journal of Neuroimmunology, 85(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1860

Badovinac V, Mostarica-Stojković MB, Dinarello C, Stošić-Grujičić S. Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells. in Journal of Neuroimmunology. 1998;85(1):null-95.
https://hdl.handle.net/21.15107/rcub_ibiss_1860 .

Badovinac, V, Mostarica-Stojković, Marija B, Dinarello, CA, Stošić-Grujičić, Stanislava, "Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells" in Journal of Neuroimmunology, 85, no. 1 (1998),
https://hdl.handle.net/21.15107/rcub_ibiss_1860 .

TY  - CONF
AU  - Stošić-Grujičić, Stanislava
AU  - Trajković, V
AU  - Badovinac, V
PY  - 1998
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1854
C3  - European Cytokine Network
T1  - Effect of leflunomide on cytokine-induced nitric oxide production in rats
IS  - 3
VL  - 9
EP  - 436
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1854
ER  - 

@conference{
author = "Stošić-Grujičić, Stanislava and Trajković, V and Badovinac, V",
year = "1998",
journal = "European Cytokine Network",
title = "Effect of leflunomide on cytokine-induced nitric oxide production in rats",
number = "3",
volume = "9",
pages = "436",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1854"
}

Stošić-Grujičić, S., Trajković, V.,& Badovinac, V.. (1998). Effect of leflunomide on cytokine-induced nitric oxide production in rats. in European Cytokine Network, 9(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1854

Stošić-Grujičić S, Trajković V, Badovinac V. Effect of leflunomide on cytokine-induced nitric oxide production in rats. in European Cytokine Network. 1998;9(3):null-436.
https://hdl.handle.net/21.15107/rcub_ibiss_1854 .

Stošić-Grujičić, Stanislava, Trajković, V, Badovinac, V, "Effect of leflunomide on cytokine-induced nitric oxide production in rats" in European Cytokine Network, 9, no. 3 (1998),
https://hdl.handle.net/21.15107/rcub_ibiss_1854 .