Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist. - Wikidata - wikimedia - TriplyDB

Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist.

Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist.

http://www.wikidata.org/entity/Q30360671

about

Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injury Function, structure and therapeutic potential of complement C5a receptors Traumatic Brain Injury and Peripheral Immune Suppression: Primer and Prospectus Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?Dealing with Danger in the CNS: The Response of the Immune System to Injury.Reduced neuronal cell death after experimental brain injury in mice lacking a functional alternative pathway of complement activation Deficiency of complement receptors CR2/CR1 in Cr2⁻/⁻ mice reduces the extent of secondary brain damage after closed head injury.Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease The level of B7 homologue 1 expression on brain DC is decisive for CD8 Treg cell recruitment into the CNS during EAE.The neural stem/progenitor cell marker nestin is expressed in proliferative endothelial cells, but not in mature vasculature.Intracerebral dendritic cells critically modulate encephalitogenic versus regulatory immune responses in the CNS.Versatility of the complement system in neuroinflammation, neurodegeneration and brain homeostasis Neurosteroids reduce inflammation after TBI through CD55 induction.The role of the anaphylatoxins in health and disease.Apolipoprotein E isoform-dependent microglia migration Complement plays an important role in spinal cord injury and represents a therapeutic target for improving recovery following trauma.Inhibition of the alternative complement activation pathway in traumatic brain injury by a monoclonal anti-factor B antibody: a randomized placebo-controlled study in mice.In situ activation of antigen-specific CD8+ T cells in the presence of antigen in organotypic brain slices.Guilty molecules, guilty minds? The conflicting roles of the innate immune response to traumatic brain injury Novel C5a regulators in inflammatory disease.An anticomplement agent that homes to the damaged brain and promotes recovery after traumatic brain injury in mice The role of inflammation in CNS injury and disease HIV-Tat regulates macrophage gene expression in the context of neuroAIDS.Neuroprotection in stroke by complement inhibition and immunoglobulin therapy.Neuroproteomics and Systems Biology Approach to Identify Temporal Biomarker Changes Post Experimental Traumatic Brain Injury in Rats.Protective effects of decay-accelerating factor on blast-induced neurotrauma in rats.The role of the complement system in CNS inflammatory diseases.MIF: a key player in cutaneous biology and wound healing.Complement in the brain.Complement activation in the injured central nervous system: another dual-edged sword?Neutrophils and viral-induced neurologic disease.Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss.Mechanisms of brain signaling during sepsis.Sepsis-associated delirium: the pro and con of C5a blockade.C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta.Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression Neuromyelitis Optica: Deciphering a Complex Immune-Mediated Astrocytopathy.Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease.Endothelial activation and chemoattractant expression are early processes in isolated blast brain injury.

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P2860

Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist.

http://www.wikidata.org/entity/Q30360671

description

2004 nî lūn-bûn

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2004 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年论文

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name

Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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type

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

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J.JNEUROIM.2004.06.003

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Journal of Neuroimmunology

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Complement C3 and C5 play crit ...... on by C5a receptor antagonist.

@en

P2093

Brendon Nacewicz

http://www.w3.org/2001/XMLSchema#string

Diane L Sewell

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Frances Liu

http://www.w3.org/2001/XMLSchema#string

Matyas Sandor

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Sinarack Macvilay

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Zsuzsa Fabry

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P2860

Complement. Second of two parts

Complement C5 in experimental autoimmune encephalomyelitis (EAE) facilitates remyelination and prevents gliosis.

A novel role of complement: mice deficient in the fifth component of complement (C5) exhibit impaired liver regeneration.

Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome.

A central role for CD4(+) T cells and RANTES in virus-induced central nervous system inflammation and demyelination

The role of complement anaphylatoxin C5a in neurodegeneration: implications in Alzheimer's disease.

Focal inflammation in the brain: role in Alzheimer's disease.

Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice.

Up-regulated production and activation of the complement system in Alzheimer's disease brain.

The proinflammatory mediators C3a and C5a are essential for liver regeneration

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55-63

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scholarly article

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10.1016/J.JNEUROIM.2004.06.003

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1-2

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155

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John D. Lambris

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2004-10-01T00:00:00Z

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8370773

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15342196

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4766842

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