A5003170013- Neuroinflammation and Neurodegeneration Mechanisms
- Multiple Sclerosis Research Studies
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Autoimmune Neurological Disorders and Treatments
- Immune Response and Inflammation
- Systemic Lupus Erythematosus Research
- Peripheral Neuropathies and Disorders
- Alzheimer's disease research and treatments
- RNA regulation and disease
- Immune Cell Function and Interaction
- Epilepsy research and treatment
- Herpesvirus Infections and Treatments
- Cytokine Signaling Pathways and Interactions
- Neurogenesis and neuroplasticity mechanisms
- Cell Adhesion Molecules Research
- S100 Proteins and Annexins
- Blood properties and coagulation
- Peroxisome Proliferator-Activated Receptors
- Neuroscience and Neuropharmacology Research
- interferon and immune responses
- Polyomavirus and related diseases
- Immune cells in cancer
- Monoclonal and Polyclonal Antibodies Research
- Platelet Disorders and Treatments
Medical University of Vienna
2016-2025
St. Josef-Hospital
2025
Jena University Hospital
2024
Inserm
2013-2023
Université de Toulouse
2023
University of Auckland
2023
Centre Hospitalier de Tourcoing
2020-2023
Université Toulouse III - Paul Sabatier
2013-2023
Centre National de la Recherche Scientifique
2013-2023
National Eye Institute
2023
Multiple sclerosis is a chronic inflammatory disease of the central nervous system, associated with demyelination and neurodegeneration. The mechanisms tissue injury are currently poorly understood, but recent data suggest that mitochondrial may play an important role in this process. Since can be triggered by reactive oxygen nitric oxide species, we analysed immunocytochemistry presence cellular location oxidized lipids DNA lesions normal-appearing white matter 30 patients multiple 24...
Classical paraneoplastic encephalitis syndromes with 'onconeural' antibodies directed to intracellular antigens, and the recently described or non-paraneoplastic encephalitides against both neural surface antigens (voltage-gated potassium channel-complexes, N-methyl-d-aspartate receptors) (glutamic acid decarboxylase-65), constitute an increasingly recognized group of immune-mediated brain diseases. Evidence for specific immune mechanisms, however, is scarce. Here, we report qualitative...
Abstract Objective Severe inflammation and astrocyte loss with profound demyelination in spinal cord optic nerves are typical pathological features of neuromyelitis optica (NMO). A diagnostic hallmark this disease is the presence serum autoantibodies against water channel aquaporin‐4 (AQP‐4) on astrocytes. Methods We induced acute T‐cell–mediated experimental autoimmune encephalomyelitis Lewis rats confronted animals an additional application immunoglobulins from AQP‐4 antibody–positive...
Multiple sclerosis is an inflammatory demyelinating disease in which active demyelination and neurodegeneration are associated with lymphocyte infiltrates the brain. However, so far little known regarding phenotype function of these infiltrating populations. In this study, we performed in-depth phenotypic characterization T B cell a large set multiple cases different lesion stages compared findings those seen inflammatory, non-inflammatory normal human controls. lesions, found dominance CD8+...
Perivascular microglia activation is a hallmark of inflammatory demyelination in multiple sclerosis (MS), but the mechanisms underlying and specific strategies to attenuate their remain elusive. Here, we identify fibrinogen as novel regulator show that targeting interaction with integrin receptor Mac-1 (αMβ2, CD11b/CD18) sufficient suppress experimental autoimmune encephalomyelitis mice retain full coagulation function. We fibrinogen, which deposited perivascularly MS plaques, signals...
Neocortical demyelination in the forebrain has recently been identified as an important pathological feature of multiple sclerosis (MS). Here we describe that cerebellar cortex is a major predilection site for demyelination, particular patients with primary and secondary progressive MS. In these patients, on average, 38.7% cortical area affected, reaching extreme examples up to 92%. Cerebellar occurs mainly band‐like manner, affecting folia. The lesions are characterized by relative axonal...
Cortical lesions constitute an important part of multiple sclerosis pathology. Although inflammation appears to play a role in their formation, the mechanisms leading demyelination and neurodegeneration are poorly understood. We aimed identify some these by combining gene expression studies with neuropathological analysis. In our study, we showed that combination inflammation, plaque-like primary cortex is specific for not seen other chronic inflammatory diseases mediated CD8-positive T...
Abstract Traumatic spinal cord injury is a devastating insult followed by progressive atrophy and neurodegeneration. Dysregulated or non-resolving inflammatory processes can disturb neuronal homeostasis drive Here, we provide an in-depth characterization of innate adaptive responses as well oxidative tissue in human traumatic lesions compared to non-traumatic control cords. In the lesion core, microglia were rapidly lost while intermediate (co-expressing pro- anti-inflammatory molecules)...
Abstract Rasmussen's encephalitis is a progressive epileptic disorder characterized by unihemispheric lymphocytic infiltrates, microglial nodules, and neuronal loss leading to the destruction of affected hemisphere. In this study, immunohistochemical evaluation specimens from 11 patients revealed infiltrates that consisted mainly CD3 + CD8 T cells. Of these cells, 7.0% lay in direct apposition MHC class I neurons. Confocal laser microscopy lymphocytes contained granzyme B polar orientation...
Lesions obtained early in the course of multiple sclerosis (MS) have been studied immunocytochemically, and compared with stages experimental lesion induced rats by intraspinal injection lipopolysaccharide. Large hemispheric or double sections were examined from patients who had died acute relapsing sclerosis. In MS exhibiting hypoxia-like lesions [Pattern III; Lucchinetti et al. Ann Neurol (2000) 47: 707–17], focal areas white matter showed mild oedema, microglial activation axonal injury...
We studied the cellular basis of self tolerance B cells specific for brain autoantigens using transgenic mice engineered to produce high titers autoantibodies against myelin oligodendrocyte glycoprotein (MOG), a surface component central nervous system myelin. generated “knock-in” by replacing germline JH locus with rearranged immunoglobulin (Ig) H chain variable (V) gene pathogenic MOG-specific monoclonal antibody. In mice, conventional reach normal numbers in bone marrow and periphery...
The gene for the beta A4-amyloid precursor protein (APP) consists of 19 exons which code a typical N- and O-glycosylated transmembrane with four extracellular domains followed by domain short cytoplasmic domain. sequence is part 16 17. Several APP isoforms can be generated alternative splicing 7 8, encoding homologies to Kunitz-type protease inhibitors MRC OX-2 antigen, respectively. mechanism pathological A4 unknown, it however critical event in Alzheimer's disease distinct from normally...
Primary rat astrocyte cultures were used to isolate a macrophage population that does not adhere the confluent glial cells. The cells multiplied vigorously in coculture with astrocytes during 14 d culture period, provided functionally active lipopolysaccharide (LPS) was either absent or present very low concentrations. Based on morphological, immunocytochemical, and pharmacological data, it concluded isolated microglia, resident macrophages of brain. findings characterized them as distinct...
Gray matter pathology is increasingly recognized as an important feature of multiple sclerosis (MS), but the nature immune response that targets gray poorly understood. Starting with a proteomics approach, we identified contactin-2/transiently expressed axonal glycoprotein 1 (TAG-1) candidate autoantigen by both autoantibodies and T helper (Th) 1/Th17 cells in MS patients. Contactin-2 its rat homologue, TAG-1, are various neuronal populations sequestered juxtaparanodal domain myelinated...
Abstract Clinical signs of experimental autoimmune encephalomyelitis (EAE) in rats can be suppressed by treatment with liposomes containing dichloromethylene diphosphonate (Cl 2 MDP liposomes). Here we investigated whether besides the blood‐borne macrophages also ED2 + perivascular cells and microglia are affected this treatment. For purpose examined central nervous system bone marrow chimeras which EAE was induced encephalitogenic T cells. Quantification cell numbers various types...
Abstract The EDI monoclonal antibody recognizes an antigen in lysosomal membranes of phagocytes. expression this cells increases during phagocytic activity. Here we describe the ED1‐immunoreactivity various stages both acute (monophasic) and chronic relapsing experimental autoimmune encephalomyelitis (EAE) Lewis rat. During first attack EAE, was present macrophages which displayed morphologic features activated microglial (i.e., with thick short processes). At ultrastructural level these...