TY  - JOUR
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Anđus, Pavle R.
AU  - Bataveljić, Danijela
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1111/ejn.15451
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4486
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1G93A rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+ . First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1G93A spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1G93A oligodendrocytes. In addition, the Ba2+ -sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1G93A spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.
PB  - Hoboken: John Wiley and Sons Inc.
T2  - European Journal of Neuroscience
T1  - Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.
IS  - 7
VL  - 54
DO  - 10.1111/ejn.15451
SP  - 6339
EP  - 6354
ER  - 

@article{
author = "Perić, Mina and Nikolić, Ljiljana and Anđus, Pavle R. and Bataveljić, Danijela",
year = "2021",
abstract = "Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1G93A rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+ . First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1G93A spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1G93A oligodendrocytes. In addition, the Ba2+ -sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1G93A spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.",
publisher = "Hoboken: John Wiley and Sons Inc.",
journal = "European Journal of Neuroscience",
title = "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.",
number = "7",
volume = "54",
doi = "10.1111/ejn.15451",
pages = "6339-6354"
}

Perić, M., Nikolić, L., Anđus, P. R.,& Bataveljić, D.. (2021). Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.. in European Journal of Neuroscience
Hoboken: John Wiley and Sons Inc.., 54(7), 6339-6354.
https://doi.org/10.1111/ejn.15451

Perić M, Nikolić L, Anđus PR, Bataveljić D. Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.. in European Journal of Neuroscience. 2021;54(7):6339-6354.
doi:10.1111/ejn.15451 .

Perić, Mina, Nikolić, Ljiljana, Anđus, Pavle R., Bataveljić, Danijela, "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis." in European Journal of Neuroscience, 54, no. 7 (2021):6339-6354,
https://doi.org/10.1111/ejn.15451 . .

TY  - JOUR
AU  - Bijelić, Dunja D.
AU  - Milićević, Katarina D.
AU  - Lazarević, Milica
AU  - Miljković, Đorđe
AU  - Bogdanović Pristov, Jelena J.
AU  - Savić, Danijela
AU  - Petković, Branka
AU  - Anđus, Pavle R.
AU  - Momčilović, Miljana
AU  - Nikolić, Ljiljana
PY  - 2020
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.24699
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32799373
UR  - https://radar.ibiss.bg.ac.rs/123456789/3859
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4006
AB  - Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naïve astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca2+ increase in astrocytes by promoting glial release of ATP. ATP propagated Ca2+ elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca2+ increase is specifically triggered by the autoreactive CD4+ T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca2+ signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.
PB  - John Wiley and Sons Inc.
T2  - Journal of Neuroscience Research
T1  - Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling
IS  - 11
VL  - 98
DO  - 10.1002/jnr.24699
SP  - 2317
EP  - 2332
ER  - 

@article{
author = "Bijelić, Dunja D. and Milićević, Katarina D. and Lazarević, Milica and Miljković, Đorđe and Bogdanović Pristov, Jelena J. and Savić, Danijela and Petković, Branka and Anđus, Pavle R. and Momčilović, Miljana and Nikolić, Ljiljana",
year = "2020",
abstract = "Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naïve astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca2+ increase in astrocytes by promoting glial release of ATP. ATP propagated Ca2+ elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca2+ increase is specifically triggered by the autoreactive CD4+ T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca2+ signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.",
publisher = "John Wiley and Sons Inc.",
journal = "Journal of Neuroscience Research",
title = "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling",
number = "11",
volume = "98",
doi = "10.1002/jnr.24699",
pages = "2317-2332"
}

Bijelić, D. D., Milićević, K. D., Lazarević, M., Miljković, Đ., Bogdanović Pristov, J. J., Savić, D., Petković, B., Anđus, P. R., Momčilović, M.,& Nikolić, L.. (2020). Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research
John Wiley and Sons Inc.., 98(11), 2317-2332.
https://doi.org/10.1002/jnr.24699

Bijelić DD, Milićević KD, Lazarević M, Miljković Đ, Bogdanović Pristov JJ, Savić D, Petković B, Anđus PR, Momčilović M, Nikolić L. Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research. 2020;98(11):2317-2332.
doi:10.1002/jnr.24699 .

Bijelić, Dunja D., Milićević, Katarina D., Lazarević, Milica, Miljković, Đorđe, Bogdanović Pristov, Jelena J., Savić, Danijela, Petković, Branka, Anđus, Pavle R., Momčilović, Miljana, Nikolić, Ljiljana, "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling" in Journal of Neuroscience Research, 98, no. 11 (2020):2317-2332,
https://doi.org/10.1002/jnr.24699 . .

TY  - JOUR
AU  - Bijelić, Dunja D.
AU  - Milićević, Katarina D.
AU  - Lazarević, Milica
AU  - Miljković, Đorđe
AU  - Bogdanović Pristov, Jelena J.
AU  - Savić, Danijela
AU  - Petković, Branka
AU  - Anđus, Pavle R.
AU  - Momčilović, Miljana
AU  - Nikolić, Ljiljana
PY  - 2020
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.24699
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32799373
UR  - https://radar.ibiss.bg.ac.rs/123456789/3859
AB  - Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naïve astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca2+ increase in astrocytes by promoting glial release of ATP. ATP propagated Ca2+ elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca2+ increase is specifically triggered by the autoreactive CD4+ T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca2+ signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.
PB  - John Wiley and Sons Inc.
T2  - Journal of Neuroscience Research
T1  - Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling
IS  - 11
VL  - 98
DO  - 10.1002/jnr.24699
SP  - 2317
EP  - 2332
ER  - 

@article{
author = "Bijelić, Dunja D. and Milićević, Katarina D. and Lazarević, Milica and Miljković, Đorđe and Bogdanović Pristov, Jelena J. and Savić, Danijela and Petković, Branka and Anđus, Pavle R. and Momčilović, Miljana and Nikolić, Ljiljana",
year = "2020",
abstract = "Interaction between autoreactive immune cells and astroglia is an important part of the pathologic processes that fuel neurodegeneration in multiple sclerosis. In this inflammatory disease, immune cells enter into the central nervous system (CNS) and they spread through CNS parenchyma, but the impact of these autoreactive immune cells on the activity pattern of astrocytes has not been defined. By exploiting naïve astrocytes in culture and CNS-infiltrated immune cells (CNS IICs) isolated from rat with experimental autoimmune encephalomyelitis (EAE), here we demonstrate previously unrecognized properties of immune cell-astrocyte interaction. We show that CNS IICs but not the peripheral immune cell application, evokes a rapid and vigorous intracellular Ca2+ increase in astrocytes by promoting glial release of ATP. ATP propagated Ca2+ elevation through glial purinergic P2X7 receptor activation by the hemichannel-dependent nucleotide release mechanism. Astrocyte Ca2+ increase is specifically triggered by the autoreactive CD4+ T-cell application and these two cell types exhibit close spatial interaction in EAE. Therefore, Ca2+ signals may mediate a rapid astroglial response to the autoreactive immune cells in their local environment. This property of immune cell-astrocyte interaction may be important to consider in studies interrogating CNS autoimmune disease.",
publisher = "John Wiley and Sons Inc.",
journal = "Journal of Neuroscience Research",
title = "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling",
number = "11",
volume = "98",
doi = "10.1002/jnr.24699",
pages = "2317-2332"
}

Bijelić, D. D., Milićević, K. D., Lazarević, M., Miljković, Đ., Bogdanović Pristov, J. J., Savić, D., Petković, B., Anđus, P. R., Momčilović, M.,& Nikolić, L.. (2020). Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research
John Wiley and Sons Inc.., 98(11), 2317-2332.
https://doi.org/10.1002/jnr.24699

Bijelić DD, Milićević KD, Lazarević M, Miljković Đ, Bogdanović Pristov JJ, Savić D, Petković B, Anđus PR, Momčilović M, Nikolić L. Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling. in Journal of Neuroscience Research. 2020;98(11):2317-2332.
doi:10.1002/jnr.24699 .

Bijelić, Dunja D., Milićević, Katarina D., Lazarević, Milica, Miljković, Đorđe, Bogdanović Pristov, Jelena J., Savić, Danijela, Petković, Branka, Anđus, Pavle R., Momčilović, Miljana, Nikolić, Ljiljana, "Central nervous system-infiltrated immune cells induce calcium increase in astrocytes via astroglial purinergic signaling" in Journal of Neuroscience Research, 98, no. 11 (2020):2317-2332,
https://doi.org/10.1002/jnr.24699 . .

TY  - CONF
AU  - Milićević, Katarina
AU  - Milošević, Milena
AU  - Božić, Iva
AU  - Lavrnja, Irena
AU  - Stevanović, Ivana
AU  - Bijelić, Dunja D.
AU  - Živković, Irena
AU  - Stević, Zorica
AU  - Anđus, Pavle R.
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5990
AB  - Introduction. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that affects motor neurons. Having in mind well documented facts that on one hand, ALS brain is under oxidative stress, and on the other that non-cell autonomous mechanisms involving glial cells contribute to the disease progression, we wanted to examine the effect of humoral factors immunoglobulins G from ALS patients (ALS IgG) on oxidative stress and antioxidative system of BV-2 microglial cell line. Methods. BV-2 cells were treated with ALS and control IgG (0.1 mg/ml). TNF-α release, oxidative stress markers and antioxidative enzymes activities were determined using biochemical assays (24 h treatment), while gene expression was determined using RT-qPCR (4 h treatment). ROS, cytosolic peroxide and pH alteration were evaluated with carboxy-H2DCFDA, HyPer and SypHer, respectively. Results. All tested ALS IgG (compared with control IgG) induced oxidative stress (rise in NO and lipid peroxidation), release of TNF-α and higher antioxidative defense (elevation of Mn- and Cu,Zn-superoxide dismutase, catalase, glutathione reductase with a decrease of glutathione peroxidase and glutathione). IgG from 4/11 ALS patients induced slow exponential rise of HyPer intensity and lower increase of SypHer intensity. None of the control IgG induced changes with neither of the indicators. Acute ROS generation was detected in 1/3 of ALS samples with carboxy-H2DCFDA. Conclusion. Our study demonstrates the potential role of inflammatory humoral factors, ALS IgGs, as triggers (via ROS generation) of the activation in microglia, known to occur in later stages of the disease.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - Serum IGG fraction from ALS patients alters redox homeostasis in the BV-2 microglial cell line
SP  - 72
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5990
ER  - 

@conference{
author = "Milićević, Katarina and Milošević, Milena and Božić, Iva and Lavrnja, Irena and Stevanović, Ivana and Bijelić, Dunja D. and Živković, Irena and Stević, Zorica and Anđus, Pavle R.",
year = "2017",
abstract = "Introduction. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that affects motor neurons. Having in mind well documented facts that on one hand, ALS brain is under oxidative stress, and on the other that non-cell autonomous mechanisms involving glial cells contribute to the disease progression, we wanted to examine the effect of humoral factors immunoglobulins G from ALS patients (ALS IgG) on oxidative stress and antioxidative system of BV-2 microglial cell line. Methods. BV-2 cells were treated with ALS and control IgG (0.1 mg/ml). TNF-α release, oxidative stress markers and antioxidative enzymes activities were determined using biochemical assays (24 h treatment), while gene expression was determined using RT-qPCR (4 h treatment). ROS, cytosolic peroxide and pH alteration were evaluated with carboxy-H2DCFDA, HyPer and SypHer, respectively. Results. All tested ALS IgG (compared with control IgG) induced oxidative stress (rise in NO and lipid peroxidation), release of TNF-α and higher antioxidative defense (elevation of Mn- and Cu,Zn-superoxide dismutase, catalase, glutathione reductase with a decrease of glutathione peroxidase and glutathione). IgG from 4/11 ALS patients induced slow exponential rise of HyPer intensity and lower increase of SypHer intensity. None of the control IgG induced changes with neither of the indicators. Acute ROS generation was detected in 1/3 of ALS samples with carboxy-H2DCFDA. Conclusion. Our study demonstrates the potential role of inflammatory humoral factors, ALS IgGs, as triggers (via ROS generation) of the activation in microglia, known to occur in later stages of the disease.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "Serum IGG fraction from ALS patients alters redox homeostasis in the BV-2 microglial cell line",
pages = "72",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5990"
}

Milićević, K., Milošević, M., Božić, I., Lavrnja, I., Stevanović, I., Bijelić, D. D., Živković, I., Stević, Z.,& Anđus, P. R.. (2017). Serum IGG fraction from ALS patients alters redox homeostasis in the BV-2 microglial cell line. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 72.
https://hdl.handle.net/21.15107/rcub_ibiss_5990

Milićević K, Milošević M, Božić I, Lavrnja I, Stevanović I, Bijelić DD, Živković I, Stević Z, Anđus PR. Serum IGG fraction from ALS patients alters redox homeostasis in the BV-2 microglial cell line. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:72.
https://hdl.handle.net/21.15107/rcub_ibiss_5990 .

Milićević, Katarina, Milošević, Milena, Božić, Iva, Lavrnja, Irena, Stevanović, Ivana, Bijelić, Dunja D., Živković, Irena, Stević, Zorica, Anđus, Pavle R., "Serum IGG fraction from ALS patients alters redox homeostasis in the BV-2 microglial cell line" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):72,
https://hdl.handle.net/21.15107/rcub_ibiss_5990 .

TY  - JOUR
AU  - Momčilović, Miljana
AU  - Stamenković, Vera
AU  - Jovanović, Miloš
AU  - Anđus, Pavle R.
AU  - Jakovčevski, Igor
AU  - Schachner, Melitta
AU  - Miljković, Đorđe
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0165572816302077
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2497
AB  - The extracellular matrix glycoprotein tenascin-C (TnC) has been increasingly appreciated as a molecule susceptibly reacting to abnormalities in the mammalian immune system. TnC expression is elevated in inflamed tissues outside the immune system, but also in lymphoid organs. It participates in the promotion of inflammatory responses. Here, the role of TnC in a paradigm of CNS autoimmunity was investigated. Experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, was induced in mice deficient in TnC (TnC−/− mice). Amelioration of EAE was observed in these mice in comparison to their wild-type (TnC+/+) littermates. Since T helper (Th)1 and Th17 cells play a dominant role in the pathogenesis of EAE, these cells were investigated in addition to analyzing locomotor functions and pro-inflammatory cytokine levels. Smaller numbers of interferon-gamma-producing Th1 cells and reduced ability of Th17 cells to produce interleukin-17 were observed in spleens of TnC−/− mice challenged by immunization with the myelin associated glycoprotein (MOG) when compared to TnC+/+ mice. There was no difference in Th1 and Th17 responses in non-immunized TnC−/− and TnC+/+ mice, thus excluding generalized immunosuppression in TnC−/− mice. These results show that TnC is important for the pathogenesis of CNS autoimmunity and that its deficiency interferes with Th1 and Th17 encephalitogenic potentials.
T2  - Journal of Neuroimmunology
T1  - Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis
VL  - 302
DO  - 10.1016/j.jneuroim.2016.12.001
SP  - 1
EP  - 6
ER  - 

@article{
author = "Momčilović, Miljana and Stamenković, Vera and Jovanović, Miloš and Anđus, Pavle R. and Jakovčevski, Igor and Schachner, Melitta and Miljković, Đorđe",
year = "2017",
abstract = "The extracellular matrix glycoprotein tenascin-C (TnC) has been increasingly appreciated as a molecule susceptibly reacting to abnormalities in the mammalian immune system. TnC expression is elevated in inflamed tissues outside the immune system, but also in lymphoid organs. It participates in the promotion of inflammatory responses. Here, the role of TnC in a paradigm of CNS autoimmunity was investigated. Experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, was induced in mice deficient in TnC (TnC−/− mice). Amelioration of EAE was observed in these mice in comparison to their wild-type (TnC+/+) littermates. Since T helper (Th)1 and Th17 cells play a dominant role in the pathogenesis of EAE, these cells were investigated in addition to analyzing locomotor functions and pro-inflammatory cytokine levels. Smaller numbers of interferon-gamma-producing Th1 cells and reduced ability of Th17 cells to produce interleukin-17 were observed in spleens of TnC−/− mice challenged by immunization with the myelin associated glycoprotein (MOG) when compared to TnC+/+ mice. There was no difference in Th1 and Th17 responses in non-immunized TnC−/− and TnC+/+ mice, thus excluding generalized immunosuppression in TnC−/− mice. These results show that TnC is important for the pathogenesis of CNS autoimmunity and that its deficiency interferes with Th1 and Th17 encephalitogenic potentials.",
journal = "Journal of Neuroimmunology",
title = "Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis",
volume = "302",
doi = "10.1016/j.jneuroim.2016.12.001",
pages = "1-6"
}

Momčilović, M., Stamenković, V., Jovanović, M., Anđus, P. R., Jakovčevski, I., Schachner, M.,& Miljković, Đ.. (2017). Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology, 302, 1-6.
https://doi.org/10.1016/j.jneuroim.2016.12.001

Momčilović M, Stamenković V, Jovanović M, Anđus PR, Jakovčevski I, Schachner M, Miljković Đ. Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology. 2017;302:1-6.
doi:10.1016/j.jneuroim.2016.12.001 .

Momčilović, Miljana, Stamenković, Vera, Jovanović, Miloš, Anđus, Pavle R., Jakovčevski, Igor, Schachner, Melitta, Miljković, Đorđe, "Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis" in Journal of Neuroimmunology, 302 (2017):1-6,
https://doi.org/10.1016/j.jneuroim.2016.12.001 . .