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 . .

TY  - JOUR
AU  - Jakovcevski, Igor
AU  - Miljković, Đorđe
AU  - Schachner, Melitta
AU  - Anđus, Pavle R
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/652
AB  - In vitro and in vivo studies on the role of tenascins have shown that the two paradigmatic glycoproteins of the tenascin family, tenascin-C (TnC) and tenascin-R (TnR) play important roles in cell proliferation and migration, fate determination, axonal pathfinding, myelination, and synaptic plasticity. As components of the extracellular matrix, both molecules show distinct, but also overlapping dual functions in inhibiting and promoting cell interactions depending on the cell type, developmental stage and molecular microenvironment. They are expressed by neurons and glia as well as, for TnC, by cells of the immune system. The functional relationship between neural and immune cells becomes relevant in acute and chronic nervous system disorders, in particular when the blood brain and blood peripheral nerve barriers are compromised. In this review, we will describe the functional parameters of the two molecules in cell interactions during development and, in the adult, in synaptic activity and plasticity, as well as regeneration after injury, with TnC being conducive for regeneration and TnR being inhibitory for functional recovery. Although not much is known about the role of tenascins in neuroinflammation, we will describe emerging knowledge on the interplay between neural and immune cells in autoimmune diseases, such as multiple sclerosis and polyneuropathies. We will attempt to point out the directions of experimental approaches that we envisage would help gaining insights into the complex interplay of TnC and TnR with the cells that express them in pathological conditions of nervous and immune systems.
T2  - Amino Acids
T1  - Tenascins and inflammation in disorders of the nervous system
IS  - 4
VL  - 44
SP  - null
EP  - 1127
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_652
ER  - 

@article{
author = "Jakovcevski, Igor and Miljković, Đorđe and Schachner, Melitta and Anđus, Pavle R",
year = "2013",
abstract = "In vitro and in vivo studies on the role of tenascins have shown that the two paradigmatic glycoproteins of the tenascin family, tenascin-C (TnC) and tenascin-R (TnR) play important roles in cell proliferation and migration, fate determination, axonal pathfinding, myelination, and synaptic plasticity. As components of the extracellular matrix, both molecules show distinct, but also overlapping dual functions in inhibiting and promoting cell interactions depending on the cell type, developmental stage and molecular microenvironment. They are expressed by neurons and glia as well as, for TnC, by cells of the immune system. The functional relationship between neural and immune cells becomes relevant in acute and chronic nervous system disorders, in particular when the blood brain and blood peripheral nerve barriers are compromised. In this review, we will describe the functional parameters of the two molecules in cell interactions during development and, in the adult, in synaptic activity and plasticity, as well as regeneration after injury, with TnC being conducive for regeneration and TnR being inhibitory for functional recovery. Although not much is known about the role of tenascins in neuroinflammation, we will describe emerging knowledge on the interplay between neural and immune cells in autoimmune diseases, such as multiple sclerosis and polyneuropathies. We will attempt to point out the directions of experimental approaches that we envisage would help gaining insights into the complex interplay of TnC and TnR with the cells that express them in pathological conditions of nervous and immune systems.",
journal = "Amino Acids",
title = "Tenascins and inflammation in disorders of the nervous system",
number = "4",
volume = "44",
pages = "null-1127",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_652"
}

Jakovcevski, I., Miljković, Đ., Schachner, M.,& Anđus, P. R.. (2013). Tenascins and inflammation in disorders of the nervous system. in Amino Acids, 44(4), null-1127.
https://hdl.handle.net/21.15107/rcub_ibiss_652

Jakovcevski I, Miljković Đ, Schachner M, Anđus PR. Tenascins and inflammation in disorders of the nervous system. in Amino Acids. 2013;44(4):null-1127.
https://hdl.handle.net/21.15107/rcub_ibiss_652 .

Jakovcevski, Igor, Miljković, Đorđe, Schachner, Melitta, Anđus, Pavle R, "Tenascins and inflammation in disorders of the nervous system" in Amino Acids, 44, no. 4 (2013):null-1127,
https://hdl.handle.net/21.15107/rcub_ibiss_652 .