Jia Newcombe

Summary

Affiliation: University College London
Country: UK

Publications

  1. ncbi Glutamate receptor expression in multiple sclerosis lesions
    Jia Newcombe
    Department of Neuroinflammation, Institute of Neurology, University College London, London, UK
    Brain Pathol 18:52-61. 2008
  2. ncbi Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis
    John S Tzartos
    Department of Neuropathology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK
    Am J Pathol 172:146-55. 2008
  3. ncbi Human brain endothelial cells endeavor to immunoregulate CD8 T cells via PD-1 ligand expression in multiple sclerosis
    Camille L Pittet
    Department of Medicine, Universite de Montreal, CRCHUM, Pavilion J, A, de Sève, 1560 Sherbrooke E, Montreal, QC, H2L 4M1, Canada
    J Neuroinflammation 8:155. 2011
  4. ncbi Extraction and proteomic analysis of proteins from normal and multiple sclerosis postmortem brain
    Jia Newcombe
    NeuroResource, Department of Neuroinflammation, 1 Wakefield Street, Institute of Neurology, University College London, London WC1N 1PJ, England
    J Chromatogr B Analyt Technol Biomed Life Sci 815:191-202. 2005
  5. ncbi Sodium channels contribute to microglia/macrophage activation and function in EAE and MS
    Matthew J Craner
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06520-8018, USA
    Glia 49:220-9. 2005
  6. ncbi Innate immune-mediated neuronal injury consequent to loss of astrocytes
    Peter J Darlington
    Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada
    J Neuropathol Exp Neurol 67:590-9. 2008
  7. ncbi Sodium channel expression within chronic multiple sclerosis plaques
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America United Spinal Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT, USA
    J Neuropathol Exp Neurol 66:828-37. 2007
  8. ncbi NKG2D-mediated cytotoxicity toward oligodendrocytes suggests a mechanism for tissue injury in multiple sclerosis
    Philippe Saikali
    Neuroimmunology Unit, Montreal Neurological Institute, Montreal, Quebec, Canada H3A 2B4
    J Neurosci 27:1220-8. 2007
  9. ncbi Chemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitment
    Markus Krumbholz
    Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany
    Brain 129:200-11. 2006
  10. ncbi Exploiting genotypic differences to identify genes important for EAE development
    Scott A Jelinsky
    Molecular Profiling and Biomarker Discover, Biological Technologies Department, Wyeth Research, 87 Cambridge Park Drive, Cambridge MA 02140, USA
    J Neurol Sci 239:81-93. 2005

Collaborators

Detail Information

Publications13

  1. ncbi Glutamate receptor expression in multiple sclerosis lesions
    Jia Newcombe
    Department of Neuroinflammation, Institute of Neurology, University College London, London, UK
    Brain Pathol 18:52-61. 2008
    ..However, they may be unable to maintain glutamate at levels low enough to protect oligodendrocytes rendered vulnerable to excitotoxic damage because of GluR1 up-regulation...
  2. ncbi Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis
    John S Tzartos
    Department of Neuropathology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK
    Am J Pathol 172:146-55. 2008
    ....
  3. ncbi Human brain endothelial cells endeavor to immunoregulate CD8 T cells via PD-1 ligand expression in multiple sclerosis
    Camille L Pittet
    Department of Medicine, Universite de Montreal, CRCHUM, Pavilion J, A, de Sève, 1560 Sherbrooke E, Montreal, QC, H2L 4M1, Canada
    J Neuroinflammation 8:155. 2011
    ..We have now investigated whether human brain endothelial cells (HBECs), which maintain the BBB, can express PD-L1 or PD-L2 and thereby modulate T cells...
  4. ncbi Extraction and proteomic analysis of proteins from normal and multiple sclerosis postmortem brain
    Jia Newcombe
    NeuroResource, Department of Neuroinflammation, 1 Wakefield Street, Institute of Neurology, University College London, London WC1N 1PJ, England
    J Chromatogr B Analyt Technol Biomed Life Sci 815:191-202. 2005
    ..This approach may be of value for the proteomic identification and quantitation of proteins which undergo disease-related changes in CNS disorders, and also for protein expression studies on normal adult and developing CNS tissues...
  5. ncbi Sodium channels contribute to microglia/macrophage activation and function in EAE and MS
    Matthew J Craner
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06520-8018, USA
    Glia 49:220-9. 2005
    ....
  6. ncbi Innate immune-mediated neuronal injury consequent to loss of astrocytes
    Peter J Darlington
    Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada
    J Neuropathol Exp Neurol 67:590-9. 2008
    ..These data suggest that non-major histocompatibility complex-restricted immune effector cells may contribute to neuron loss in neuroinflammatory disorders indirectly through injury of glia...
  7. ncbi Sodium channel expression within chronic multiple sclerosis plaques
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America United Spinal Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT, USA
    J Neuropathol Exp Neurol 66:828-37. 2007
    ..6 and NCX in acute lesions but independent of coexpression of these 2 molecules in chronic lesions...
  8. ncbi NKG2D-mediated cytotoxicity toward oligodendrocytes suggests a mechanism for tissue injury in multiple sclerosis
    Philippe Saikali
    Neuroimmunology Unit, Montreal Neurological Institute, Montreal, Quebec, Canada H3A 2B4
    J Neurosci 27:1220-8. 2007
    ..These results imply that NKG2D-NKG2D ligand interaction can potentially contribute to cytotoxic responses mediated by activated immune effector cells in the inflamed CNS, as observed in multiple sclerosis...
  9. ncbi Chemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitment
    Markus Krumbholz
    Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany
    Brain 129:200-11. 2006
    ..Therefore, both CXCL13 and CXCR5 may be promising therapeutic targets in multiple sclerosis...
  10. ncbi Exploiting genotypic differences to identify genes important for EAE development
    Scott A Jelinsky
    Molecular Profiling and Biomarker Discover, Biological Technologies Department, Wyeth Research, 87 Cambridge Park Drive, Cambridge MA 02140, USA
    J Neurol Sci 239:81-93. 2005
    ....
  11. ncbi Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger
    Matthew J Craner
    Department of Neurology and Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 101:8168-73. 2004
    ..6 and Na+/Ca2+ exchanger is associated with axonal degeneration in MS...
  12. ncbi Annexin II/p11 is up-regulated in Purkinje cells in EAE and MS
    Matthew J Craner
    Department of Neurology and PVA/EPVA Center for Neuroscience Research, Yale University School of Medicine, 333 Cedar Street, P.O. Box 208018, New Haven, CT 06520-8018, USA
    Neuroreport 14:555-8. 2003
    ..8 within Purkinje cells perturbs the temporal pattern of impulse generation in these cells, our results extend the evidence for an acquired channelopathy which interferes with cerebellar function in MS...