Research Topics
| Ingo KleiterSummaryAffiliation: University of Regensburg Country: Germany Publications
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Detail Information
Publications
Intraventricular cytarabine in a case of idiopathic hypertrophic pachymeningitisI Kleiter
University of Regensburg, Department of Neurology, Universitatsstrasse 84, 93042 Regensburg, Germany
J Neurol Neurosurg Psychiatry 75:1346-8. 2004....- Autonomic involvement in tick-borne encephalitis (TBE): report of five casesIngo Kleiter
Department of Neurology, University of Regensburg, Universitätsstr 84, D 93042 Regensburg, Germany
Eur J Med Res 11:261-5. 2006..Tick-borne encephalitis (TBE) is a viral infection of the CNS with significant acute and long-term morbidity. Dysfunction of the autonomic nervous system may be a potentially harmful complication of TBE... - Delayed humoral immunity in a patient with severe tick-borne encephalitis after complete active vaccinationI Kleiter
Dept of Neurology, University of Regensburg, Universitätsstr 84, 93042, Regensburg, Germany
Infection 35:26-9. 2007..We report on a 54-year-old patient who had received his last booster vaccination 3 years before developing a severe TBE with delayed induction and longterm persistence of anti-TBEV-IgM-antibodies... - A lightning strike to the head causing a visual cortex defect with simple and complex visual hallucinationsIngo Kleiter
Department of Neurology, University of Regensburg, Universitätsstr 84, 93042 Regensburg, Germany
J Neurol Neurosurg Psychiatry 78:423-6. 2007..Using the European Cooperation for Lightning Detection network, a meteorological system for lightning surveillance, the exact geographical location and nature of the lightning flash were retrospectively retraced... - Early changes on electroencephalography in natalizumab-associated progressive multifocal leucoencephalopathyIngo Kleiter
Department of Neurology, University Medical Center Regensburg, Germany
Mult Scler 16:749-53. 2010..Functional neurological deficits may precede imaging features and should prompt early consideration of progressive multifocal leucoencephalopathy... - Smad7 in T cells drives T helper 1 responses in multiple sclerosis and experimental autoimmune encephalomyelitisIngo Kleiter
Department of Neurology, University Medical Centre Regensburg, Universitatsstrasse 84, 93053 Regensburg, Germany
Brain 133:1067-81. 2010..Since a Smad7 deletion in T cells leads to immunosuppression, Smad7 may be a potential new therapeutic target in multiple sclerosis... - Novel role for SLPI in MOG-induced EAE revealed by spinal cord expression analysisAndre M Mueller
Department of Neurology, University of Regensburg, Franz Josef Strauss Allee 11, 93053 Regensburg, Germany
J Neuroinflammation 5:20. 2008.... - Aquaporin 4 antibody positive central nervous system autoimmunity and multiple sclerosis are characterized by a distinct profile of antibodies to herpes virusesJohann Sellner
Department of Neurology, Klinikum rechts der Isar, Technische Universitat Munchen, Munchen, Germany
Neurochem Int 57:662-7. 2010..Whether these findings reflect an epi-phenomenon of autoimmune disorders or indicate a disease-specific deregulated virus-host interaction needs to be examined in further studies... - Inhibition of Smad7, a negative regulator of TGF-beta signaling, suppresses autoimmune encephalomyelitisIngo Kleiter
Department of Neurology, University of Regensburg, Universitaetsstr 84, 93053 Regensburg, Germany
J Neuroimmunol 187:61-73. 2007..Smad7 inhibition thus represents a novel systemic treatment strategy for autoimmune CNS inflammation, targeting TGF-beta signaling without TGF-beta-associated toxicity... - Failure of natalizumab to prevent relapses in neuromyelitis opticaIngo Kleiter
Department of Neurology, University Medical Center Regensburg, Regensburg, Germany
Arch Neurol 69:239-45. 2012..To describe first experiences with the integrin inhibitor natalizumab, given to patients with suspected relapsing-remitting multiple sclerosis (MS) who were later diagnosed with aquaporin 4-positive neuromyelitis optica (NMO)... - Targeting fibroblast growth factor-inducible-14 signaling protects from chronic relapsing experimental autoimmune encephalomyelitisA M Mueller
Department of Neurology, University of Regensburg, Universitaetsstr 84, 93053 Regensburg, Germany
J Neuroimmunol 159:55-65. 2005..Purified IgG from TWEAK- or Fn14-vaccinated rats prevented TWEAK-induced production of CCL2 by endothelial cells. Blocking Fn14 signaling represents a novel approach with potential for the treatment of CNS autoimmunity...