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Molecular and Cellular Neuroscience, ISSN 1044-7431, 2005, Volume 29, Issue 3, pp. 381 - 393
‘Protective autoimmunity’ refers to a well-controlled anti-self response that helps the body resist neurodegeneration. The response is mediated by autoimmune T... 
PROINFLAMMATORY CYTOKINE | NEUROPROTECTIVE AUTOIMMUNITY | MULTIPLE-SCLEROSIS | ALZHEIMERS-DISEASE | MACROPHAGES | GLUTAMATE | CENTRAL-NERVOUS-SYSTEM | SELF-ANTIGEN | NEUROSCIENCES | T-CELLS | GROWTH-FACTOR-I | Amyloid beta-Peptides - pharmacology | Gliosis - therapy | Transcriptional Activation - drug effects | Gliosis - physiopathology | Hippocampus - drug effects | Lipopolysaccharides - antagonists & inhibitors | Insulin-Like Growth Factor I - drug effects | Neurodegenerative Diseases - immunology | Lipopolysaccharides - immunology | Histocompatibility Antigens Class II - drug effects | Insulin-Like Growth Factor I - immunology | Interleukin-4 - pharmacology | Lymphocyte Activation - immunology | Encephalitis - physiopathology | Microglia - immunology | Autoimmunity - immunology | T-Lymphocytes - drug effects | Tumor Necrosis Factor-alpha - immunology | Gliosis - immunology | Organ Culture Techniques | Animals, Newborn | Cell Line | Encephalitis - therapy | Hippocampus - immunology | Microglia - drug effects | Cells, Cultured | Rats | Encephalitis - immunology | Neurodegenerative Diseases - therapy | Down-Regulation - drug effects | Rats, Sprague-Dawley | Interleukin-4 - immunology | Amyloid beta-Peptides - antagonists & inhibitors | Animals | Histocompatibility Antigens Class II - immunology | Neurodegenerative Diseases - physiopathology | Tumor Necrosis Factor-alpha - drug effects | Down-Regulation - immunology | Lymphocyte Activation - drug effects | Interferon-gamma - immunology | Lipopolysaccharides - pharmacology | Amyloid beta-Peptides - immunology | T-Lymphocytes - immunology | Transcriptional Activation - physiology | Hippocampus - physiopathology | Autoimmunity - drug effects | Interferon-gamma - pharmacology
Journal Article
Stroke, ISSN 0039-2499, 09/2011, Volume 42, Issue 9, pp. 2589 - 2594
Background and Purpose-Activation of Notch worsens ischemic brain damage as antisense knockdown or pharmacological inhibition of the Notch pathway reduces the... 
apoptosis | focal ischemia | brain ischemia | inflammation | neuroregeneration | neuroprotection | CELLS | BRAIN-DAMAGE | PROLIFERATION | DEATH | CLINICAL NEUROLOGY | STROKE | TUMOR-NECROSIS-FACTOR | PERIPHERAL VASCULAR DISEASE | NF-KAPPA-B | UP-REGULATION | Amyloid Precursor Protein Secretases - genetics | Inflammation - pathology | Microglia - metabolism | Coculture Techniques | Brain Ischemia - genetics | Immunity, Innate - genetics | NF-kappa B - metabolism | Brain Ischemia - immunology | Inflammation - metabolism | Cell Nucleus - metabolism | Microglia - pathology | Gliosis - immunology | Active Transport, Cell Nucleus - genetics | Cytokines - genetics | Gliosis - genetics | Mice, Transgenic | Inflammation - therapy | Amyloid Precursor Protein Secretases - metabolism | Cell Nucleus - genetics | Active Transport, Cell Nucleus - immunology | Mice | Receptor, Notch1 - antagonists & inhibitors | Oligopeptides - pharmacology | Receptor, Notch1 - genetics | Cell Nucleus - immunology | Amyloid Precursor Protein Secretases - immunology | Gliosis - therapy | NF-kappa B - immunology | Brain Ischemia - metabolism | Gliosis - pathology | Microglia - immunology | Inflammation Mediators - metabolism | Cytokines - immunology | Inflammation Mediators - immunology | Cell Line | Gene Expression Regulation - genetics | Gene Expression Regulation - immunology | Brain Ischemia - therapy | Gliosis - metabolism | Receptor, Notch1 - immunology | Inflammation - immunology | Receptor, Notch1 - metabolism | Immunity, Innate - immunology | Animals | NF-kappa B - genetics | Brain Ischemia - pathology | Inflammation - genetics | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Cytokines - biosynthesis | Index Medicus
Journal Article
Glia, ISSN 0894-1491, 05/2006, Volume 53, Issue 7, pp. 688 - 695
Toll‐like receptors (TLRs) are innate immunity receptors that are expressed on a wide range of cell types, including CNS glial cells. In general, TLR... 
astrocytes | inflammation | Toll‐like receptors | neuroprotection | Toll-like receptors | Neuroprotection | Inflammation | Astrocytes | CELLS | DOUBLE-STRANDED-RNA | toll-like receptors | CNS | KAPPA-B | INDUCTION | NEUROSCIENCES | INHIBITION | GROWTH | NEUROTROPHINS | EXPRESSION | BRAIN | Humans | Male | Gliosis - physiopathology | Neuroprotective Agents - metabolism | Encephalitis - physiopathology | Astrocytes - immunology | Growth Substances - immunology | Encephalitis - metabolism | Interleukins - immunology | Cytoprotection - drug effects | Aged, 80 and over | Toll-Like Receptor 4 - agonists | Female | Growth Inhibitors - biosynthesis | Gliosis - immunology | Interleukins - biosynthesis | Cytoprotection - immunology | Growth Inhibitors - pharmacology | Astrocytes - drug effects | Cell Survival - drug effects | Endothelial Cells - metabolism | Gliosis - metabolism | Cells, Cultured | Encephalitis - immunology | Toll-Like Receptor 3 - immunology | Toll-Like Receptor 3 - agonists | Toll-Like Receptor 4 - immunology | Cell Survival - immunology | Down-Regulation - drug effects | Toll-Like Receptor 3 - metabolism | Toll-Like Receptor 4 - metabolism | Endothelial Cells - immunology | Up-Regulation - drug effects | Growth Inhibitors - immunology | Up-Regulation - immunology | Down-Regulation - immunology | Growth Substances - pharmacology | Aged | Growth Substances - biosynthesis | Cytokines - pharmacology | Astrocytes - metabolism | Endothelial Cells - drug effects
Journal Article
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2007, Volume 26, Issue 3, pp. 497 - 511
Abstract We investigated the involvement of the complement cascade during epileptogenesis in a rat model of temporal lobe epilepsy (TLE), and in the chronic... 
Neurology | Human | Epileptogenesis | Rat | Astrocytes | Neurons | Immunocytochemistry | Microarray | Hippocampus | PCR | Microglia | rat | hippocampus | ALZHEIMERS-DISEASE | STATUS EPILEPTICUS | immunocytochemistry | neurons | FOCAL CORTICAL DYSPLASIA | NEUROSCIENCES | RAT MODEL | GLIONEURONAL TUMORS | SPONTANEOUS SEIZURES | microarray | MULTIPLE-SCLEROSIS | HIPPOCAMPAL SCLEROSIS | epileptogenesis | GENE-EXPRESSION | astrocytes | human | microglia | INTRACTABLE EPILEPSY | Microglia - metabolism | Complement C3d - genetics | Complement C5b - immunology | Humans | Middle Aged | Status Epilepticus - immunology | Male | Status Epilepticus - genetics | RNA, Messenger - metabolism | Complement C1q - metabolism | Complement System Proteins - metabolism | Complement C3d - metabolism | Encephalitis - physiopathology | Epilepsy, Temporal Lobe - genetics | Gliosis - immunology | Disease Models, Animal | Gliosis - genetics | Complement C5b - genetics | Rats | Encephalitis - immunology | Complement C3c - genetics | Hippocampus - pathology | Complement C1q - genetics | Rats, Sprague-Dawley | Up-Regulation - immunology | Adolescent | Complement C3c - immunology | Hippocampus - physiopathology | Astrocytes - metabolism | Complement C3d - immunology | Complement C1q - immunology | Complement System Proteins - immunology | Epilepsy, Temporal Lobe - physiopathology | Epilepsy, Temporal Lobe - immunology | Gliosis - physiopathology | Complement C5b - metabolism | Microglia - immunology | Astrocytes - immunology | Complement C3c - metabolism | Adult | Complement System Proteins - genetics | Female | Hippocampus - immunology | Encephalitis - genetics | RNA, Messenger - genetics | Up-Regulation - genetics | Animals | Status Epilepticus - physiopathology | Aged | Epilepsy
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2006, Volume 22, Issue 2, pp. 312 - 322
Chemokine receptors represent promising targets to attenuate inflammatory responses and subsequent secondary damage after brain injury. We studied the response... 
Neuroprotection | CINC-1 | MIP-2 | CXCR2 | CXCL1 | Leukocytes | CXCL2 | Brain injury | Microglia | CONTROLLED CORTICAL IMPACT | BONE-MARROW | MICROGLIAL CELLS | NEUROSCIENCES | MACROPHAGE-INFLAMMATORY PROTEIN-2 | NONPEPTIDE ANTAGONIST | brain injury | CONSTITUTIVE EXPRESSION | MULTIPLE-SCLEROSIS | MARROW-DERIVED CELLS | NEUTROPHIL MIGRATION | neuroprotection | leukocytes | CENTRAL-NERVOUS-SYSTEM | microglia | Neuroimmunomodulation - immunology | Chemokines, CXC - immunology | Rats, Wistar | Nerve Degeneration - physiopathology | Brain Injuries - complications | Male | Gliosis - physiopathology | Nerve Degeneration - metabolism | Cell Movement - immunology | Encephalitis - physiopathology | Microglia - immunology | Encephalitis - metabolism | Brain Damage, Chronic - metabolism | Gliosis - immunology | Chemokines - immunology | Disease Models, Animal | Biomarkers - metabolism | Ectodysplasins | Gliosis - metabolism | Rats | Encephalitis - immunology | Membrane Proteins - immunology | Nerve Degeneration - immunology | Receptors, Interleukin-8B - immunology | Cell Survival - immunology | Tumor Necrosis Factors - immunology | Brain Damage, Chronic - physiopathology | Cell Differentiation - immunology | Animals | Up-Regulation - immunology | Down-Regulation - immunology | Receptors, Interleukin-8B - metabolism | Chemokines, CXC - metabolism | Chemokine CXCL2 | Brain Damage, Chronic - immunology | Chemokine CXCL1 | Brain | Brain damage | Laws, regulations and rules | Neurons | Injuries
Journal Article
Journal of Neuropathology and Experimental Neurology, ISSN 0022-3069, 12/2008, Volume 67, Issue 12, pp. 1137 - 1148
The expression patterns of tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a pleiotropic cytokine with proinflammatory and cell death-inducing... 
Cortical lesions | Multiple sclerosis | Inflammation | Cytokines | Microglia | KAPPA-B ACTIVATION | MESSENGER-RNA EXPRESSION | TNF SUPERFAMILY | PATHOLOGY | NEUROSCIENCES | LESIONS | CLINICAL NEUROLOGY | WEAK INDUCER | TUMOR-NECROSIS-FACTOR | CELL FOLLICLES | CENTRAL-NERVOUS-SYSTEM | MONOCLONAL-ANTIBODIES | MULTIFUNCTIONAL CYTOKINE | Tumor Necrosis Factors - genetics | Meninges - immunology | Humans | Blood-Brain Barrier - physiopathology | Cerebral Cortex - pathology | Gliosis - physiopathology | TWEAK Receptor | Cerebral Cortex - physiopathology | Gliosis - pathology | Multiple Sclerosis - physiopathology | Encephalitis - physiopathology | Microglia - immunology | Astrocytes - immunology | Gliosis - immunology | Macrophages - immunology | Receptors, Tumor Necrosis Factor - genetics | Receptors, Tumor Necrosis Factor - metabolism | Blood-Brain Barrier - immunology | Cerebral Arteries - immunology | Meninges - pathology | Myelin Sheath - immunology | Myelin Sheath - pathology | Brain - physiopathology | Tumor Necrosis Factors - metabolism | Encephalitis - pathology | Receptors, Tumor Necrosis Factor - analysis | Cerebral Arteries - physiopathology | Encephalitis - immunology | Tumor Necrosis Factors - immunology | Blood-Brain Barrier - pathology | Cytokine TWEAK | B-Lymphocytes - immunology | Up-Regulation - immunology | Cerebral Cortex - immunology | Cerebral Arteries - pathology | Brain - pathology | Multiple Sclerosis - immunology | Multiple Sclerosis - pathology | Chemotaxis, Leukocyte - immunology | Brain - immunology
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 11/2006, Volume 99, Issue 4, pp. 1263 - 1272
It is well established that inflammatory changes contribute to brain ageing, and an increased concentration of proinflammatory cytokine, interleukin‐1β... 
interleukin‐1β | interferon‐γ | long‐term potentiation | age | interleukin‐18 | microglial activation | Interleukin-18 | Interferon-γ | Interleukin-1β | Long-term potentiation | Age | Microglial activation | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | NEUROSCIENCES | PROTEIN-KINASES | CELL-DEATH | IN-VITRO | interleukin-1 beta | interleukin-18 | MOUSE MODEL | AGING HUMAN BRAIN | CENTRAL-NERVOUS-SYSTEM | RAT HIPPOCAMPUS | interferon-gamma | long-term potentiation | Memory Disorders - physiopathology | Microglia - metabolism | Interleukin-18 - immunology | Interleukin-1alpha - immunology | Rats, Wistar | Minocycline - pharmacology | Memory Disorders - metabolism | Interleukin-1alpha - metabolism | Male | Gliosis - physiopathology | Interferon-gamma - metabolism | Dentate Gyrus - physiopathology | CD40 Antigens - metabolism | Encephalitis - physiopathology | Microglia - immunology | Long-Term Potentiation - drug effects | Encephalitis - metabolism | Long-Term Potentiation - physiology | Gliosis - immunology | B7-2 Antigen - immunology | Cytokines - immunology | Biomarkers - metabolism | Dentate Gyrus - metabolism | Cytokines - metabolism | Microglia - drug effects | Anti-Inflammatory Agents - pharmacology | Intercellular Adhesion Molecule-1 - immunology | Gliosis - metabolism | Rats | Encephalitis - immunology | Memory Disorders - immunology | B7-2 Antigen - metabolism | Hippocampus - metabolism | Intercellular Adhesion Molecule-1 - metabolism | Animals | Aging - physiology | Interferon-gamma - immunology | Hippocampus - physiopathology | CD40 Antigens - immunology | Interleukin-18 - metabolism | Brain | Neurology | Cytokines | Long term | Rodents
Journal Article
Journal of Neuroinflammation, ISSN 1742-2094, 08/2009, Volume 6, Issue 1, pp. 23 - 23
Background: Lyme neuroborreliosis (LNB) may present as meningitis, cranial neuropathy, acute radiculoneuropathy or, rarely, as encephalomyelitis. We... 
BORRELIA-BURGDORFERI | TUMOR-NECROSIS-FACTOR | NONHUMAN PRIMATE MODEL | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | RHESUS-MONKEY | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | CENTRAL-NERVOUS-SYSTEM | MENINGEAL INFLAMMATION | IMMUNOLOGY | CEREBROSPINAL-FLUID | NEUROSCIENCES | FACTOR-ALPHA | Lyme Neuroborreliosis - pathology | Neurons - pathology | Spinal Cord Diseases - physiopathology | Nerve Degeneration - physiopathology | Ganglia, Spinal - physiopathology | Gliosis - physiopathology | Macaca mulatta | Encephalitis - physiopathology | Lyme Neuroborreliosis - immunology | Spinal Cord - pathology | Leukocytosis - physiopathology | Lyme Neuroborreliosis - physiopathology | Neuroglia - immunology | Radiculopathy - physiopathology | Leukocytosis - microbiology | Gliosis - immunology | Ganglia, Spinal - immunology | Spinal Cord Diseases - immunology | Neurons - microbiology | Brain - physiopathology | Leukocytosis - immunology | Nerve Degeneration - microbiology | Neurons - immunology | Radiculopathy - microbiology | Encephalitis - immunology | Nerve Degeneration - immunology | Neuroglia - microbiology | Gliosis - microbiology | Spinal Cord - immunology | Meningitis - immunology | Animals | Apoptosis - immunology | Spinal Cord Diseases - microbiology | Ganglia, Spinal - pathology | Brain - pathology | Antibodies - blood | Chemokines - metabolism | Spinal Cord - physiopathology | Meningitis - microbiology | Meningitis - physiopathology | Brain - immunology | Encephalitis - microbiology | Radiculopathy - immunology | Prevention | Lyme disease | Usage | Care and treatment | Fluorescent antibody technique | Research | Immunofluorescence | T cells | Health aspects | Apoptosis
Journal Article
Glia, ISSN 0894-1491, 03/2002, Volume 37, Issue 4, pp. 314 - 327
In this study, we investigate the expression of fractalkine (CX3CL1) and the fractalkine receptor (CX3CR1) in the naive rat and mouse central nervous system... 
chemokine | in vivo | brain | inflammation | chemokine receptor | Chemokine | Brain | In vivo | Chemokine receptor | Inflammation | CELLS | MICROGLIAL ACTIVATION | LEUKOCYTE RECRUITMENT | MEMBRANE-BOUND CHEMOKINE | NEUROSCIENCES | CXCR1 | LIPOPOLYSACCHARIDE | CENTRAL-NERVOUS-SYSTEM | RAT-BRAIN | MONOCLONAL-ANTIBODIES | PROSTAGLANDIN E-2 | Immunohistochemistry | Microglia - metabolism | Male | Brain - metabolism | Scrapie - physiopathology | Chemotaxis, Leukocyte - drug effects | Neuroglia - immunology | Receptors, HIV - immunology | Neurons - metabolism | Chemokines, CX3C - immunology | Gliosis - immunology | Receptors, Cytokine - metabolism | Acute Disease | Brain - physiopathology | Rats | Encephalitis - immunology | Chemokines, CX3C - pharmacology | Up-Regulation - immunology | Mice | Chemotaxis, Leukocyte - immunology | CX3C Chemokine Receptor 1 | Chronic Disease | Astrocytes - metabolism | Rats, Wistar | Gliosis - chemically induced | Neurons - cytology | Membrane Proteins - pharmacology | Neuroglia - drug effects | Microglia - immunology | Astrocytes - immunology | Encephalitis - metabolism | Scrapie - immunology | Membrane Proteins - metabolism | Astrocytes - drug effects | Microglia - drug effects | Gliosis - metabolism | Mice, Inbred C57BL | Neurons - immunology | Chemokines, CX3C - metabolism | Membrane Proteins - immunology | Scrapie - metabolism | Up-Regulation - drug effects | Chemokine CX3CL1 | Animals | Receptors, HIV - metabolism | Neuroglia - metabolism | Receptors, Cytokine - immunology | Encephalitis - chemically induced | Brain - immunology
Journal Article