Figure 7 VEGF as a mediator of neuroinflammatory disease

Slides:



Advertisements
Similar presentations
Pathologic Basis of Disease Neuropathology - 1. Major cells of the CNS Neurons Glial cells: -astrocytes -oligodendrocytes -ependymal cells -microglial.
Advertisements

A Feline-specific Blood Brain Barrier. Feline Immunodeficiency Virus Lentivirus Natural infection in cats worldwide Induces disease Animal model of HIV.
Teaching NeuroImages Neurology Resident and Fellow Section © 2013 American Academy of Neurology A 51-year-old woman with triplegia and blindness.
DENDRITES CELL BODY AXON MYELIN SHEATH GLIAL CELL / GLIA NODE OF RANVIER.
Harry Irving, Hung Jiew Lee, John Parratt
Nat. Rev. Neurol. doi:10/1038/nrneurol
Lymphatic system of the brain
Nat. Rev. Neurol. doi: /nrneurol
Figure 3 Life expectancy at birth in all countries included
Figure 1 Perivenous distribution of multiple sclerosis lesions
Volume 18, Issue 1, Pages (February 2011)
Nat. Rev. Neurol. doi: /nrneurol
Inducing Angiogenesis
Paul M. George, Gary K. Steinberg  Neuron 
Nat. Rev. Neurol. doi: /nrneurol
Figure Model contrasting the potential role of antibodies to myelin oligodendrocyte glycoprotein (MOG) or aquaporin-4 (AQP4) in opticospinal inflammationMOG-specific.
Roopa Bhat, Lawrence Steinman  Neuron 
Nat. Rev. Neurol. doi: /nrneurol
Nat. Rev. Neurol. doi: /nrneurol
Nat. Rev. Neurol. doi: /nrneurol
Figure 3 Proportion of patients for whom NEDA
Figure 5 Number of AHSCT procedures for
Figure 4 Neuromyelitis optica spectrum disorder brain lesions
Figure 1 Physiological metabolism of Aβ in the brain and periphery
Figure 2 Co-stimulatory receptors as immunomodulatory targets
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 1 Percent positivity by clinical feature Overall, 6
Nat. Rev. Urol. doi: /nrurol
Nat. Rev. Neurol. doi: /nrneurol
Figure 3 Hypothetical mechanisms of smoking-associated
Figure 1 Principles of therapeutic ultrasound
Figure 1 Clinical correlates of neurodegeneration in MS
Nat. Rev. Neurol. doi: /nrneurol
Figure 4 Lifestyle and environmental factors affect
Figure 1 Evolution of multiple sclerosis
Nat. Rev. Neurol. doi: /nrneurol
Chander Raman, Ph.D. February 2018
Figure 5 Role of VEGF in stroke
Figure 2 Carotid artery inflammation detected using 68Ga-DOTATATE-PET
Figure 6 Vascular dysfunction in epilepsy
Figure 3 VEGF in neurodegenerative disease
Figure 2 Brain-infiltrating immune cells mainly consist of CD8+ memory T cells Immunofluorescence staining of brain-infiltrating immune cells. Brain-infiltrating.
Figure 3 Biologics that attenuate effector responses in the kidney
Figure 1 Integrative model of NMO/SD pathogenesis
Figure 1 Biomarkers associated with different clinical phases in MS
Jason D. Ulrich, Tien-Phat Huynh, David M. Holtzman  Neuron 
Nat. Rev. Neurol. doi: /nrneurol
Figure 2 Logistical requirements for autologous
Figure 1 The VEGF family of growth factors
Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)
Nat. Rev. Urol. doi: /nrurol
Figure 2 Key transport properties of the capillary endothelium
Nat. Rev. Neurol. doi: /nrneurol
Robyn S. Klein, Christopher A. Hunter  Immunity 
Nat. Rev. Neurol. doi: /nrneurol
Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.
Figure 2 Immune changes in peripheral blood of pregnant patients with NMO Immune changes in peripheral blood of pregnant patients with NMO (A) Interleukin.
Figure 3 Blood–brain barrier breakdown promotes neurodegeneration
Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.
Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.
Nat. Rev. Neurol. doi: /nrneurol
Figure 2 Hypothetical model of temporal brain changes
Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.
Figure 2 Natalizumab increases expression of proinflammatory genes and cytokines by CD49d+ memory CD4 cells Natalizumab increases expression of proinflammatory.
Figure 1. MBP-specific IFN-γ+ but not IL-17+ frequencies are significantly different between patients with MS and HCs MBP-specific IFN-γ+ but not IL-17+
Figure 4 Treponema pallidum invasion
Deletion of HtrA1 does not alter vascular or immune cell morphology or distribution in the young-adult mouse neocortex. Deletion of HtrA1 does not alter.
Schematic diagram of mechanisms of stroke-induced immunosuppression with NK cells as an example. Schematic diagram of mechanisms of stroke-induced immunosuppression.
Figure 1. Initiation of vasculitic lesions in small vessels by ANCA-activating cytokine-primed neutrophils in the wrong place and at the wrong time. Figure.
Presentation transcript:

Figure 7 VEGF as a mediator of neuroinflammatory disease Figure 7 | VEGF as a mediator of neuroinflammatory disease. a | Healthy brain vessels possess a functional blood–brain barrier (BBB) to support the cells of the surrounding brain parenchyma, while protecting it from immune cells and harmful substances in the blood. b | At early stages of neuroinflammatory disease, vessel barriers become weakened, allowing egress of immune cells that attack targets such as aquaporin-4-positive BBB-associated astrocytes in the case of neuromyelitis optica (NMO), or oligodendrocytes in multiple sclerosis (MS). Activated microglia secrete IL-1β, which induces vascular endothelial growth factor (VEGF) expression in astrocytes. c | Prolonged VEGF elevation increases angiogenic sprouting and causes breakdown of the BBB, a hallmark of advanced stages of neuroinflammatory disease. Inflammatory reactions against the respective target cells (BBB-associated astrocytes in NMO; oligodendrocytes in MS) cause death of the target cells and secondary neuronal apoptosis. Lange, C. et al. (2016) Vascular endothelial growth factor: a neurovascular target in neurological diseases Nat. Rev. Neurol. doi:10.1038/nrneurol.2016.88