Neuroscience in Denmark

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General information

Name (center, department, group or other)
Neuroimmunology (Owens) group, Neurobiology, SDU
Contact name
Trevor Owens
Contact email
Contact title
22. September 2015

Brief description of research activities

The Neuroimmunology group study pathogenic mechanisms of inflammatory diseases of the central nervous system (CNS), such as multiple sclerosis (MS) and neuromyelitis optica (NMO). We mainly focus to mouse models and we use histological, flow cytometric, molecular, (RNA-analysis ) and tissue culture methods to evaluate immuno- and neuropathogenesis in genetically-modified mice. We study interactions between the immune system and glial cells of the nervous system, both those that lead to pathology as well as with regulatory and protective outcomes. We are particularly interested in translating clinical observations to experimental analyses and we collaborate with groups in Region Syddanmark to understand how innate and adaptive immune cells and mediators contribute to neurological disease.
Immune, Glial, Multiple sclerosis, Neuromyelitis optica, animal models

Research tools and techniques

Experimental models of neuroinflammation; flow cytometry; RT-PCR; fluorescence microscopy

Scientific Personnel

No of Associate Professors/Postdocs: 3
No of PhD students: 4
Other: 7

Key references from within the last 5 years

1.Khorooshi, R. and Owens, T. 2010. Injury-induced type I interferon signaling regulates inflammatory responses in the CNS. J. Immunol. 185: 1258-1264.

2.Toft-Hansen, H., Fuchtbauer, LM, and Owens, T. 2011. Inhibition of reactive astrocytosis in established experimental autoimmune encephalomyelitis favors infiltration by myeloid cells over T cells and enhances severity of disease. Glia 59:166-176.

3.Asgari, N., R. Khorooshi, S. Lillevang, & T. Owens. 2013. Complement-dependent pathogenicity of brain-specific antibodies in cerebrospinal fluid. J. Neuroimmunol. 254:76- 82. Epub 2012/10/04.

4.Khorooshi, R., A. Wlodarczyk, N. Asgari, & T. Owens. 2013. Neuromyelitis optica-like pathology is dependent on type I interferon response. Exp Neurol 247: 744-747.

5. Mony, JT, Khorooshi R, & Owens, T. 2014. MOG extracellular domain (p1-125) triggers elevated frequency of CXCR3+ Th1 CD4+ T cells in CNS and induces greater incidence of severe EAE. MS Journal (DOI: 10.1177/1352458514524086).

6. Wlodarczyk, A., Løbner, M., Cedile, O., & Owens, T. 2014. Comparison of microglia and infiltrating CD11c+ cells as antigen presenting cells for T cell proliferation and cytokine response. J. Neuroinflammation 11:57.

7.Cedile, O, Løbner, M, Toft-Hansen, H, Frank, I, Wlodarczyk, A, Irla, M, & Owens, T. 2014 Thymic CCL2 influences induction of T-cell tolerance. J Autoimmun http://

8.Khorooshi R, Morch MT, Holm TH, Berg CT, Dieu RT, Draeby D, Issazadeh-Navikas S, Weiss S, Lienenklaus S, Owens T (2015) Induction of endogenous Type I interferon within the central nervous system plays a protective role in experimental autoimmune encephalomyelitis. Acta Neuropathol 130: 107-118 Doi 10.1007/s00401-015-1418-z

9. Asgari N, Berg CT, Mørch MT, Khorooshi R, Owens T (2015) Cerebrospinal fluid aquaporin-4-immunoglobulin G disrupts blood brain barrier. Annals of Clinical and Translational Neurology 2: 857-863 Doi 10.1002/acn3.221
Scherfigsvej 7
2100 Copenhagen Ø
Tel. +45 39 12 80 00
CVR-nr. 11 81 49 13
Nils Axelsen Ralf Hemmingsen Lauritz Holm-Nielsen Ralf Hemmingsen Jens Oddershede Jens Frederik Rehfeld Anders Bjørklund