Deutscher Akademischer AustauschdienstPPP 57142471 (to PA and IJ)

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Deutscher Akademischer AustauschdienstPPP 57142471 (to PA and IJ)

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Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis

Momčilović, Miljana; Stamenković, Vera; Jovanović, Miloš; Anđus, Pavle R.; Jakovčevski, Igor; Schachner, Melitta; Miljković, Đorđe

(2017)

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 . .
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