Research output per year
Research output per year
PhD
Academic qualifications
1974: B.Sc., McGill University, Montreal, Canada
1977:M.Sc., McGill University, Montreal, Canada
1981:PhD, University of Ottawa, Canada
Postdoctoral training: University College London 1981-1984 (NA Mitchison); Walter and Eliza Hall Institute, Melbourne 1984-1987 (JFAP Miller).
Relevant Professional Positions and Employment
1987 - Appointed to faculty, McGill University, Montreal
2001 - 2006 Professor, McGill University
2004 - Professor, Univ. of Southern Denmark (SDU), Odense, Denmark.
2006 - Adjunct Professor, McGill University
2010 - 2023 Head of Research, Neurobiology Dept, Inst of Molecular Medicine, SDU
Research Funding
Danish Agency for Research and Innovation, Scleroseforeningen, Lundbeckfonden, NovoNordiskfonden, EU Horizon2020 Marie-Sklodowska Curie, Carlsbergfondet.
Lab members: Reza Khorooshi, Jonathan Krieger, Bita Ramazani, Rouhin Belal, Dorte Overgaard Brorsen
PUBLICATIONS: 186 total, 133 peer-reviewed.
Research areas
Neuroimmunology, central nervous system inflammation and glial response, with reference to Mutliple sclerosis (see Owens group here)
Positions
We do not have funded PhD or postdoc positions but we always welcome bright and interested candidates who will apply for funds to join one of our projects
Selected activities
•Head of Research, Neurobiology Dept, Inst of Molecular Medicine, SDU - 2010-2023
•President, Scandinavian Society for Immunology – 2015-2020
•Editorial Board for: J Neuropathol Exp Neurol - 2005-2017; Glia - 2010-present; Scand J Immunol - 2016-present (Assoc Editor 2023 -)
Selected papers (from 186 total)
• Kronborg Hansen, A.K., Dubik, M., Marczynska, J., Ojha, B., Nistal-Villán, E., González Aseguinolaza, G., Arengoth, D.S., Owens, T., Khorooshi, R. 2022. Targeting signaling pathway downstream of RIG-I/MAVS in the CNS stimulates production of endogenous type I IFN and suppresses EAE. International Journal of Molecular Sciences 23:19. Doi: 10.3390/ijms231911292
• Dieu RS, Wais V, Sørensen MZ, Marczynska J, Dubik M, Kavan S, Thomassen M, Burton M, Kruse T, Khorooshi R, Owens T: Central Nervous System-Endogenous TLR7 and TLR9 Induce Different Immune Responses and Effects on Experimental Autoimmune Encephalomyelitis. Frontiers in Neuroscience 2021, 15.
• Dubik, M., J. Marczynska, M.T. Mørch, G. Webster, K.N. Jensen, A. Wlodarczyk, R. Khorooshi, and T. Owens. 2021. Innate Signaling in the CNS Prevents Demyelination in a Focal EAE Model. Frontiers in Neuroscience 15: Doi 10.3389/fnins.2021.682451.
• Morch MT, Khorooshi R, Marczynska J, Dubik M, Nielsen S, Nieland JD, Asgari N, Owens T (2021) Mitochondria-A target for attenuation of astrocyte pathology. J Neuroimmunol 358: 577657 Doi 10.1016/j.jneuroim.2021.577657
• Soerensen SF, Wirenfeldt M, Wlodarczyk A, Moerch MT, Khorooshi R, Arengoth DS, Lillevang ST, Owens T, Asgari N (2021) An Experimental Model of Neuromyelitis Optica Spectrum Disorder-Optic Neuritis: Insights Into Disease Mechanisms. Front Neurol 12: 703249 Doi 10.3389/fneur.2021.703249
• Wlodarczyk A, Khorooshi R, Marczynska J, Holtman IR, Burton M, Jensen KN, Blaabjerg M, Meyer M, Thomassen M, Eggen BJL, Asgari N, Owens T. 2021. Type I interferon-activated microglia are critical for neuromyelitis optica pathology. Glia 69: 943-953. Doi 10.1002/glia.23938
• Benmamar-Badel, A., T. Owens, and A. Wlodarczyk. 2020. Protective microglial subset in development, aging and disease: lessons from transcriptomic studies. Frontiers in Immunology 11:43. Doi 10.3389/fimmu.2020.00430.
• Khorooshi, R., J. Marczynska, R.S. Dieu, V. Wais, C.R. Hansen, S. Kavan, M. Thomassen, M. Burton, T. Kruse, G.A. Webster, and T. Owens. 2020. Innate signaling within the central nervous system recruits protective neutrophils. Acta Neuropathologica Communications 8:2 doi: 10.1186/s40478-019-0876-2.
• Khorooshi R, Tofte-Hansen EU, Tygesen C, Montañana-Rosell R, Limburg HL, Marczynska, J, Asgari N, Steckelings UM, and Owens T. 2020. Angiotensin AT2-receptor induced interleukin-10 attenuates neuromyelitis optica spectrum disorder-like pathology. Mult Scler 26:1187-1196 doi: 10.1177/1352458519860327.
•Wlodarczyk A, Benmamar-Badel A, Cédile O, Jensen KN, Kramer I, Elsborg NB, and Owens T. 2018. CSF1R stimulation promotes increased neuroprotection by CD11c+ microglia in EAE. Frontiers Cell. Neurosci. 12: doi: 10.3389/fncel.2018.00523.
•Mørch, M, Forsberg Sørensen, S, Khorooshi, R, Asgari, N, Owens, T. 2018. Selective localization of IgG from cerebrospinal fluid to brain parenchyma. J Neuroinflammation 15:110. doi:10.1186/s12974-018-1159-8
•Wlodarczyk A, Holtman IR, Krueger M, Yogev N, Bruttger J, Khorooshi, R, Benmamar-Badel, A, de Boer-Bergsma JJ, Martin,NA, Karram K, Kramer, I, Boddeke EWGM, Waisman A, Eggen BJL and Owens T. (2017). A novel microglial subset plays a key role in myelinogenesis in developing brain. EMBO J. doi: 10.15252/embj.201696056
•Berg, CT, Khorooshi, R, Asgari, N. and Owens, T. (2017). Influence of Type I IFN signaling on anti-MOG antibody-mediated demyelination. J. Neuroinflammation 14:127
•Wlodarczyk, A, Cédile, O, Jensen, KN, Jasson, A, Mony, JT, Khorooshi, R, and Owens, T. 2015. Pathologic and protective roles for microglial subsets and bone marrow- and blood-derived myeloid cells in central nervous system inflammation. Frontiers in Immunology 6:463 doi: 10.3389/fimmu.2015.00463
•Asgari N, Berg CT, Mørch MT, Khorooshi R, and Owens T. 2015. Cerebrospinal Fluid Aquaporin-4-IgG induces blood brain barrier breakdown. Ann Clin Trans Neurol, 2: 857-863 DOI: 101002/acn3221:n/a-n/a
•Khorooshi, R., Mørch, M, Berg, CT, Holm, TH, Dieu, RT, Dræby, D, Issazadeh-Navikas, S, Weiss, S, Lienenklaus, S and Owens, T. 2015. Induction of endogenous Type I interferon within the central nervous system plays a protective role in experimental autoimmune encephalomyelitis. Acta Neuropathologica, 130:107-118.
•Cédile, 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 55:73-85.
•Mony, JT, Khorooshi R, & Owens, T. 2014. Chemokine receptor expression by inflammatory T cells in EAE. Front. Cell. Neurosci. 8:187. doi: 10.3389/fncel.2014.00187.
•Wlodarczyk, A., Løbner, M., Cédile, O., and Owens, T. 2014. Comparison of microglia and infiltrating CD11c+ cells as antigen presenting cells for T cell proliferation and cytokine response. J Neuroinflammation 11:57-65.
•Khorooshi R, Wlodarczyk A, Asgari N, Owens T. 2013. Neuromyelitis optica-like pathology is dependent on type I interferon response. Exp Neurol, 247:744-747.
•Owens, T., Khorooshi, R., Wlodarczyk, A. and Asgari, N. (2013), Interferons in the central nervous system: A few instruments play many tunes. Glia. doi: 10.1002/glia.22608
•Khorooshi, R., Wlodarczyk, A., Asgari, N., Owens, T., 2013. Neuromyelitis optica-like pathology is dependent on type I interferon response. Exp Neurol. doi: 10.1016/j.expneurol.2013.02.005.
•Asgari, N., R. Khorooshi, S. Lillevang, and T. Owens. 2013. Complement-dependent pathogenicity of brain-specific antibodies in cerebrospinal fluid. J. Neuroimmunol. 254:76-82. Epub 2012/10/04.
•Maiorino, C., R Khorooshi, F Ruffini, M Løbner, A Bergami, L Garzetti, G Martino, T Owens, and R Furlan. 2012. Lentiviral-mediated administration of IL-25 in the CNS induces alternative activation of microglia. Gene Therapy Epub 2012/08/03.
•Holm, TH., D, Draeby, and T. Owens. 2012. Microglia are required for astroglial Toll-like receptor 4 response, and for optimal Toll-like receptor 2 and 3 response. Glia 60:630-638
•Finsen, B. and Owens, T. 2011. Innate immune responses in central nervous system inflammation. FEBS Letts 585:3806-3812.
•Khorooshi, R., and T. Owens. 2010. Injury-induced type I interferon signaling regulates inflammatory responses in the CNS. J Immunol. 185:1258-1264
•Khorooshi, R., Babcock, A.A., and Owens, T. 2008. NFkappaB-driven STAT2 and CCL2 expression in astrocytes in response to brain injury. J. Immunol. 181: 7284-7291
•Babcock AA, Wirenfeldt M, Holm, T, Nielsen, HH, Dissing-Olesen, L, Toft-Hansen H, Millward JM, Landmann R, Rivest S, Finsen B, and Owens T. 2006. Toll-like receptor 2 signaling in response to brain injury: an innate bridge to neuroinflammation. J Neurosci 26:12826-12837.
We study inflammation in the central nervous system, using animal models to dissect cellular and molecular interactions that underlie pathogenesis of diseases such as Multiple sclerosis (MS) and Neuromyelitis optica (NMO). MS is considered to be primarily a T-cell-mediated autoimmune inflammatory disease, with associated neurodegeneration, whereas NMO is considered to be an antibody-mediated inflammatory disease with demyelination. Both diseases show activation of microglia, and astrocytes are the main target of antibody in NMO. The interactions of these cells with T cells macrophages and antibodies are the major focus of our research.
For more information see www.sdu.dk/immed/nb-ow
Researcher, Næstved-Slagelse-Ringsted Hospitals
1. Jun 2021 → 30. Sept 2023
Research output: Contribution to journal › Journal article › Research › peer-review
Research output: Contribution to journal › Journal article › Research › peer-review
Research output: Contribution to journal › Journal article › Communication
Research output: Contribution to conference without publisher/journal › Poster › Research
Research output: Contribution to journal › Conference abstract in journal › Research
Owens, T. (Participant)
Activity: Attending an event › Conference organisation or participation
Owens, T. (Participant)
Activity: Attending an event › Organisation or participation in workshops, courses or seminars
Owens, T. (Participant)
Activity: Attending an event › Organisation or participation in workshops, courses or seminars
Owens, T. (Guest lecturer)
Activity: Talks and presentations › Conference presentations
Owens, T. (Guest lecturer)
Activity: Talks and presentations › Guest lectures, external teaching and course activities at other universities
31/05/2023
1 Media contribution
Press/Media: Press / Media
31/05/2023
1 Media contribution
Press/Media: Press / Media
25/10/2021
1 Media contribution
Press/Media: Press / Media
15/01/2020
1 Media contribution
Press/Media: Press / Media