Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis
2017
Authors:
Momčilović, MiljanaStamenković, Vera
Jovanović, Miloš
Anđus, Pavle R.
Jakovčevski, Igor
Schachner, Melitta
Miljković, Đorđe
Document Type:
Article (Published version)
,
© 2016 Elsevier B.V.
Metadata
Show full item recordAbstract:
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.
Keywords:
Tenascin-C; Experimental autoimmune encephalomyelitis; T helper cells; Interferon-gamma; Interleukin-17; Multiple sclerosisSource:
Journal of Neuroimmunology, 2017, 302, 1-6Funding / projects:
- Cellular and molecular mechanisms of recovery of rats from experimental autoimmune encephalomyelitis (RS-MESTD-Basic Research (BR or ON)-173035)
- Molecular mechanisms of physiological and pharmacological control of inflammation and cancer (RS-MESTD-Basic Research (BR or ON)-173013)
- Biomarkers in neurodegenerative and malignant processes (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41005)
- Deutscher Akademischer AustauschdienstPPP 57142471 (to PA and IJ)
DOI: 10.1016/j.jneuroim.2016.12.001
ISSN: 0165-5728
PubMed: 27974153
WoS: 000392675000001
Scopus: 2-s2.0-85007393144
URI
http://linkinghub.elsevier.com/retrieve/pii/S0165572816302077https://radar.ibiss.bg.ac.rs/handle/123456789/2497