• Multiple Sclerosis
    • Hans P Lassmann
    • Hans P Lassmann: Influence Statistics

      Hans P Lassmann

      Hans P Lassmann

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      Center for Brain Research, Medical University of Vienna, Wien, Austria | Medical University Vienna | Department of Neuroimmunology, Center for Brain Research, Medical ...

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      Hans P Lassmann:Expert Impact

      Concepts for whichHans P Lassmannhas direct influence:Multiple sclerosis,Central nervous,Autoimmune encephalomyelitis,Spinal cord,Experimental autoimmune,Neuromyelitis optica,Oligodendrocyte glycoprotein.

      Hans P Lassmann:KOL impact

      Concepts related to the work of other authors for whichfor which Hans P Lassmann has influence:Multiple sclerosis,Central nervous,Spinal cord,Neuromyelitis optica,Autoimmune encephalomyelitis,White matter,Neurodegenerative diseases.

      KOL Resume for Hans P Lassmann


      Center for Brain Research, Medical University of Vienna, Wien, Austria


      Medical University Vienna


      Department of Neuroimmunology, Medical University, Vienna, Austria.


      Neuroimmunology Department, Center for Brain Research, Medical University of Vienna, Wien, Austria

      Center for Brain Research, Medical University of Vienna.


      Institute of Brain Pathology, Medical University, Vienna


      From the Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands (JD, NvD, BAH, YSK); Department of Neuroscience, University Medical Center, University of Groningen, Groningen, The Netherlands (JD, BAH, JDL); Medical University of Vienna, Center for Brain Research, Vienna, Austria (JB, HL); Centre for Neuroregeneration, University of Edinburgh, Edinburgh, United Kingdom (GRC, DJM); and Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands (SMAvdP, JvH)

      Department of Neurology (P.K., M.P., H.-J.H., M.M.), Institute of Neuropathology (C.M.), University Hospital Magdeburg; German Center for Neurodegenerative Diseases (DZNE) Magdeburg (P.K.), Germany; Institute of Neurology (M.B., G.G.K., R.H.), Department of Pediatric and Adolescent Medicine (M.B.), Department of Neurology (P.R.), Division of Neuroradiology and Musculoskeletal Radiology (C.M.), Department of Biomedical Imaging and Image-guided Therapy, and Department of Neuroimmunology (H.L.), Center for Brain Research, Medical University of Vienna, Austria; Department of Neuropathology (I.M., W.B.), University Medical Center Göttingen; Leibniz Institute for Neurobiology (H.-J.H.), Magdeburg; Department of Neurology (M.M.), MEDIAN NRZ Flechtingen, Germany; Clinical Department of Neurology (M.R.), Innsbruck Medical University, Austria; Neuroimmunology (K.-P.W., F.L.), Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, Kiel/Lübeck; Department of Neurology (K.-P.W.), University Hospital Schleswig-Holstein, Lübeck; and Department of Neurology (F.L.), University Hospital Schleswig-Holstein, Kiel, Germany.

      Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Wien, Austria.


      Department of Neuroimmunology, Center for Brain Research, Medical University Vienna, Spitalgasse 4, A-1090 Vienna, Austria

      Abteilung für Neuroimmunologie, Medizinische Universität Wien, Wien, Österreich


      From the Departments of Neurology (FA-D) and Radiology (WK), SMZ-Ost Donauspital; Karl Landsteiner Institute for Neuroimmunological and Neurodegenerative Disorders (FA-D, WK); Institute of Neurology (RH, HB) and Center for Brain Research, Department of Neuroimmunology (HL), Medical University of Vienna, Vienna, Austria; and Neuroimmunology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom (PW, AV).

      Clinical Department of Neurology (F.D.P., M.R., R.B., K.S., E.S., T.B.) and Department of Neuroradiology (P.R.), Medical University of Innsbruck; Institute of Neurology (R.H.) and Center for Brain Research (H.L.), Medical University of Vienna, Austria; and Departments of Neurology and Multiple Sclerosis Therapeutics (D.S., K.F.), Tohoku University Graduate School of Medicine, Sendai, Japan.

      Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria


      Department of Neuroimmunology, Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria


      From the Departments of Infectious and Tropical Diseases (G.M.-B., A.D., P.M., B.M.), Neuroradiology (V.C.), and Pathology (E.U.-C., M.-B.D.), Toulouse University Hospital; INSERM U1043–CNRS UMR 5282 (G.M.-B., L.T.M., R.S.L.), Centre de Physiopathologie Toulouse-Purpan; Université Toulouse III (G.M.-B., V.C., E.U.-C., P.M., M.-B.D., B.M., L.T.M., R.S.L.), France; Center for Brain Research (J.B., H.L.), Medical University of Vienna, Austria; INSERM (E.U.-C., M.-B.D.), CRCT U1087, Toulouse; and CNRS, LCC (B.M.), Université de Toulouse, France.

      Department of Neuroimmunology, Centre for Brain Research, Medical University of Vienna, Austria


      Medical University Vienna Center for Brain Research Vienna Austria

      These authors contributed equally to this work


      1 Centre for Brain Research, Medical University of Vienna, A-1090 Wien, Austria


      Department of Neuroimmunology, Center for Brain Research, and

      Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria

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      Sample of concepts for which Hans P Lassmann is among the top experts in the world.
      Concept World rank
      hartley eae #1
      staging astrocytopathy #1
      demyelination oligodendrocyte #1
      development messenger #1
      antibody eae #1
      developmental regulation ehk1 #1
      eae17 genetic heterogeneity #1
      rats mog eae #1
      data mitochondrial injury #1
      nfp phf #1
      classical eae #1
      matter oligodendrocyte #1
      acd35 #1
      drb11501 experimental epitopes #1
      tnf central nervous #1
      iifn #1
      normal recipient rats #1
      granulocyte infiltration loss #1
      chp characteristics mice #1
      cellular cytotoxicity gbs #1
      hypoxialike tissue injury #1
      cyclooxygenase inhibitor ibuprofen #1
      eae5 pia4 #1
      demyelinating disease cns #1
      blood stream rats #1
      eae eae23b #1
      promoter remyelination #1
      mog‐induced eae #1
      dementia brain lesions #1
      keith lassmann #1
      comparative neuropathology #1
      rabs cerebrospinal fluid #1
      elisa mog #1
      gangliosideantiserum #1
      cx3cl1 mog eae #1
      abs 2 patients #1
      nervous eye #1
      brain multiple #1
      interest2 #1
      bovine endocrine #1
      protective function studies #1
      tnfr1 eae #1
      rats betapeptides amyloid #1
      genes eae23b #1
      destruction myelin sheaths #1
      dqb10602 plp #1
      activation central nervous #1
      cns enmo #1
      antigens antigens head #1
      mag deficiency #1
      Sign-in to see all concepts, it's free!

      Prominent publications by Hans P Lassmann

      KOL-Index: 18333

      BACKGROUND: The CC chemokine receptors CCR1, CCR2 and CCR5 are critical for the recruitment of mononuclear phagocytes to the central nervous system (CNS) in multiple sclerosis (MS) and other neuroinflammatory diseases. Mononuclear phagocytes are effector cells capable of phagocytosing myelin and damaging axons. In this study, we characterize the regional, temporal and cellular expression of CCR1, CCR2 and CCR5 mRNA in the spinal cord of rats with myelin oligodendrocyte ...

      Known for Chemokine Receptors | Central Nervous | Ccr1 Ccr2 | Spinal Cord | Expression Regulation
      KOL-Index: 16995

      BACKGROUND: There is consensus that experimental autoimmune encephalomyelitis (EAE) can be mediated by myelin specific T cells of Th1 as well as of Th17 phenotype, but the contribution of either subset to the pathogenic process has remained controversial. In this report, we compare functional differences and pathogenic potential of "monoclonal" T cell lines that recognize myelin oligodendrocyte glycoprotein (MOG) with the same transgenic TCR but are distinguished by an IFN-γ producing ...

      Known for Th17 Cells | Autoimmune Encephalomyelitis | Knockout Mice | Adoptive Transfer | Ifn Γ
      KOL-Index: 16123

      Classical paraneoplastic encephalitis syndromes with 'onconeural' antibodies directed to intracellular antigens, and the recently described paraneoplastic or non-paraneoplastic encephalitides and antibodies against both neural surface antigens (voltage-gated potassium channel-complexes, N-methyl-d-aspartate receptors) and intracellular antigens (glutamic acid decarboxylase-65), constitute an increasingly recognized group of immune-mediated brain diseases. Evidence for specific immune ...

      Known for Intracellular Antigens | Encephalitides Antibodies | Neuronal Loss | Methyl Aspartate | Gated Potassium
      KOL-Index: 16100

      EAE, an animal model for MS, is a Th17 and Th1-cell-mediated autoimmune disease, but the mechanisms leading to priming of encephalitogenic T cells in autoimmune neuroinflammation are poorly understood. To investigate the role of plasmacytoid DC (pDC) in the initiation of autoimmune Th17- and Th1-cell responses and EAE, we depleted pDC with anti-pDC Ag-1 (anti-PDCA1) mAb prior to immunization of C57BL/6 mice with myelin oligodendrocyte glycoprotein (MOG). pDC-depleted mice developed less ...

      Known for Th17 Cells | Type Ifn | Animal Model | Autoimmune Neuroinflammation | Glycoprotein Mog
      KOL-Index: 15921

      Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the CNS. A recent study identified 4 patterns of demyelination in active MS lesions. The characteristics of pattern II lesions suggested a primary inflammatory mechanism of myelin injury, while pattern III lesions showed features consistent with dying-back oligodendrogliopathy. The recruitment, differentiation, and activation of mononuclear phagocytes are dependent on the expression of chemokine receptors. Using ...

      Known for Chemokine Receptors | Mononuclear Phagocytes | Ccr1 Ccr5 | Pattern Iii | Sclerosis Lesions
      KOL-Index: 15890

      The histone deacetylases HDAC1 and HDAC2 are crucial regulators of chromatin structure and gene expression, thereby controlling important developmental processes. In the mouse brain, HDAC1 and HDAC2 exhibit different developmental stage- and lineage-specific expression patterns. To examine the individual contribution of these deacetylases during brain development, we deleted different combinations of Hdac1 and Hdac2 alleles in neural cells. Ablation of Hdac1 or Hdac2 by Nestin-Cre had no ...

      Known for Hdac1 Hdac2 | Brain Development | Gene Expression | Neural Cells | Chromatin Structure
      KOL-Index: 15046

      The pathogenic potential of autoimmune T cell responses to nonmyelin autoantigens was investigated in the Lewis rat using the astrocyte-derived calcium binding protein S100 beta, as a model nonmyelin autoantigen. The Lewis rat mounts a vigorous RT1B1 (major histocompatibility complex class II) restricted autoimmune response to an immunodominant S100 beta epitope (amino acid residues 76-91). The adoptive transfer of S100 beta-specific T cell lines induced a severe inflammatory response in ...

      Known for S100 Beta | Lewis Rat | Experimental Autoimmune | Adoptive Transfer | Cns Eae
      KOL-Index: 14786

      We dissected the requirements for disease induction of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis in MHC (RT1 in rat) congenic rats with overlapping MOG peptides. Immunodominance with regard to peptide-specific T cell responses was purely MHC class II dependent, varied between different MHC haplotypes, and was linked to encephalitogenicity only in RT1.B(a)/D(a) rats. Peptides derived from the MOG sequence 91-114 were able to induce overt ...

      Known for Mhc Class | Oligodendrocyte Glycoprotein | Autoimmune Encephalomyelitis | Experimental Epitopes | Central Nervous
      KOL-Index: 14764

      Multiple sclerosis is a chronic inflammatory disease of the central nervous system, associated with demyelination and neurodegeneration. The mechanisms of tissue injury are poorly understood, but recent data suggest that mitochondrial injury may play an important role in this process. Mitochondrial injury can be triggered by reactive oxygen and nitric oxide species, and we recently provided evidence for oxidative damage of oligodendrocytes and dystrophic axons in early stages of active ...

      Known for Mitochondrial Injury | Nadph Oxidase | Multiple Sclerosis | Activated Microglia | Tissue Damage
      KOL-Index: 14202

      Previous authors have shown that the transverse relaxivity R(2)* and frequency shifts that characterize gradient echo signal decay in magnetic resonance imaging are closely associated with the distribution of iron and myelin in the brain's white matter. In multiple sclerosis, iron accumulation in brain tissue may reflect a multiplicity of pathological processes. Hence, iron may have the unique potential to serve as an in vivo magnetic resonance imaging tracer of disease pathology. To ...

      Known for Multiple Sclerosis | 7 Tesla | Magnetic Resonance | Brain Tissue | Iron Myelin
      KOL-Index: 14184

      A monoclonal antibody (8-18C5) directed against myelin/oligodendrocyte glycoprotein (MOG) induced demyelination in aggregating brain cell cultures. With increasing doses of anti-MOG antibody in the presence of complement, myelin basic protein (MBP) concentration decreased in a dose-related manner. A similar, albeit less pronounced, effect was observed on specific activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase. In the absence of complement, anti-MOG antibody did not induce ...

      Known for Brain Cell Cultures | Oligodendrocyte Glycoprotein | Monoclonal Antibody | Demyelination Induced | Myelin Sheath
      KOL-Index: 14058

      Experimental autoimmune encephalomyelitis (EAE) was induced with myelin oligodendrocyte glycoprotein (MOG(1-125)) in CD4(-/-) and CD8(-/-) DBA/1 mice. Both gene-deleted mice developed clinical signs of EAE, albeit milder than in wild-type mice, suggesting that both CD4(+) and CD8(+) cells participate in disease development. Demyelination and inflammation in the central nervous system was reduced in the absence of CD8(+) T cells. Antibody depletion of CD4(+) cells completely protected ...

      Known for Cd8 Cells | Autoimmune Encephalomyelitis | Eae Cd4 | Inbred Dba Mice | Central Nervous
      KOL-Index: 13939

      In multiple sclerosis (MS), diffuse degenerative processes in the deep grey matter have been associated with clinical disabilities. We performed a systematic study in MS deep grey matter with a focus on the incidence and topographical distribution of lesions in relation to white matter and cortex in a total sample of 75 MS autopsy patients and 12 controls. In addition, detailed analyses of inflammation, acute axonal injury, iron deposition and oxidative stress were performed. MS deep ...

      Known for Deep Grey Matter | Multiple Sclerosis | Demyelination Neurodegeneration | Inflammation Iron | Caudate Nucleus
      KOL-Index: 13936

      BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is associated with local activation of microglia and astroglia, infiltration of activated macrophages and T cells, active degradation of myelin and damage to axons and neurons. The proposed role for CX3CL1 (fractalkine) in the control of microglia activation and leukocyte infiltration places this chemokine and its receptor CX3CR1 in a potentially strategic position to control key ...

      Known for Cx3cr1 Expression | Cells Microglia | Autoimmune Encephalomyelitis | Cx3cl1 Cns | Myelin Oligodendrocyte

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      Center for Brain Research, Medical University of Vienna, Wien, Austria | Medical University Vienna | Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria. | From the Neuroimmunology Unit (L.C.-N., S.

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