title: Tenascin-C deficiency protects mice from experimental autoimmune encephalomyelitis.
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.
authors.affiliation: Department of Immunology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Serbia.
authors.forename: Miljana
authors.initials: M
authors.lastname: Momčilović
authors.affiliation: Department of Physiology and Biochemistry, Faculty of Biology, University of Belgrade, Serbia.
authors.forename: Vera
authors.initials: V
authors.lastname: Stamenković
authors.affiliation: Department of Physiology and Biochemistry, Faculty of Biology, University of Belgrade, Serbia.
authors.forename: Miloš
authors.initials: M
authors.lastname: Jovanović
authors.affiliation: Department of Physiology and Biochemistry, Faculty of Biology, University of Belgrade, Serbia.
authors.forename: Pavle R
authors.initials: PR
authors.lastname: Andjus
authors.affiliation: Experimental Neurophysiology, German Center for Neurodegenerative Diseases, Bonn, Germany; Institute for Molecular and Behavioral Neuroscience, University of Cologne, Cologne, Germany; Zentrum für Molekulare Neurobiologie, Universitätskrankenhaus Hamburg-Eppendorf, Universität Hamburg, Martinistr. 52, D-20246 Hamburg, Germany.
authors.forename: Igor
authors.initials: I
authors.lastname: Jakovčevski
authors.affiliation: Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, USA; Center for Neuroscience, Shantou University Medical College, 22 Xin Ling Road, Shantou 515041, P.R. China.
authors.forename: Melitta
authors.initials: M
authors.lastname: Schachner
authors.affiliation: Department of Immunology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Serbia. Electronic address: georgije_zw@yahoo.com.
authors.forename: Đorđe
authors.initials: Đ
authors.lastname: Miljković
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000378:metabolism* / Q000517:prevention & control*; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D019063:Tenascin / Q000172:deficiency* / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D019063:Tenascin
keywords: Experimental autoimmune encephalomyelitis; Interferon-gamma; Interleukin-17; Multiple sclerosis; T helper cells; Tenascin-C