P Gasque

Summary

Affiliation: Cardiff University
Country: UK

Publications

  1. ncbi Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activities
    Philippe Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
    Mol Neurobiol 25:1-17. 2002
  2. ncbi Regulation by complement C3a and C5a anaphylatoxins of cytokine production in human umbilical vein endothelial cells
    Tiphaine Monsinjon
    Laboratory of Immunology, INSERM U519, IFRMP23, University of Rouen, France
    FASEB J 17:1003-14. 2003
  3. ncbi Molecular and cellular insights into the coxsackie-adenovirus receptor: role in cellular interactions in the stem cell niche
    Mathieu Hauwel
    Department of Medical Biochemistry and Immunology, Brain Inflammation and Immunity Group BIIG, Cardiff University, Heath Park, UK
    Brain Res Brain Res Rev 48:265-72. 2005
  4. ncbi Complement components of the innate immune system in health and disease in the CNS
    P Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
    Immunopharmacology 49:171-86. 2000
  5. ncbi Complement: a unique innate immune sensor for danger signals
    Philippe Gasque
    Brain Inflammation and Immunity Group BIIG, Department of Medical Biochemistry and Immunology, College of Medicine, University of Wales, Cardiff CF144XN, UK
    Mol Immunol 41:1089-98. 2004
  6. ncbi The receptor for complement anaphylatoxin C3a is expressed by myeloid cells and nonmyeloid cells in inflamed human central nervous system: analysis in multiple sclerosis and bacterial meningitis
    P Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, United Kingdom
    J Immunol 160:3543-54. 1998
  7. pmc Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis
    S K Singhrao
    Department of Medical Biochemistry, Brain Inflammation and Immunity Group, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    Am J Pathol 157:905-18. 2000
  8. ncbi Endothelial cells, megakaryoblasts, platelets and alveolar epithelial cells express abundant levels of the mouse AA4 antigen, a C-type lectin-like receptor involved in homing activities and innate immune host defense
    Y D Dean
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, GB
    Eur J Immunol 31:1370-81. 2001
  9. ncbi Role of complement in inflammation and injury in the nervous system
    B P Morgan
    University of Wales College of Medicine, Cardiff, UK
    Exp Clin Immunogenet 14:19-23. 1997
  10. ncbi Differential expression of individual complement regulators in the brain and choroid plexus
    S K Singhrao
    Department of Pathology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    Lab Invest 79:1247-59. 1999

Collaborators

  • Bryan Paul Morgan
  • S K Singhrao
  • C L Harris
  • Karen Francis
  • Eamon P McGreal
  • P Wang
  • W H Evans
  • Johan van Beek
  • A Ischenko
  • M Griffiths
  • Masashi Mizuno
  • Hubert Vaudry
  • Nobunao Ikewaki
  • C Speth
  • Mathieu Hauwel
  • Kristina Elward
  • Y D Dean
  • Riina Oksjoki
  • Sandrine Bes-Houtmann
  • Jean François Jégou
  • Duncan S Cole
  • Philippe Chan
  • Emeline Furon
  • Jennifer Brady
  • Gabor G Kovacs
  • Tiphaine Monsinjon
  • E Oviedo-Orta
  • T Monsinjon
  • Franck Festy
  • James W Neal
  • Petri T Kovanen
  • Satu Helske
  • Marc Fontaine
  • Henri Caillens
  • Regis Roche
  • Laurence Hoareau
  • Markku O Pentikainen
  • Christian Lefebvre d'Hellencourt
  • Maya Cesari
  • Pirjo Vehmaan-Kreula
  • Marie Therese Schouft
  • Petri Laine
  • Marie Paule Gonthier
  • Mikko I Mäyränpää
  • Timothy R Hughes
  • Jim Neal
  • Jim W Neal
  • Cecile Canova
  • Marin Guentchev
  • James Neal
  • Nagarajan Sadakar
  • Michaela Strohschneider
  • Herbert Budka
  • James W Ironside
  • Thomas Strobel
  • Elisabeth Lindeck-Pozza
  • Marc C Fontaine
  • Jennifer J Brady
  • M Fontaine
  • H Akatsu

Detail Information

Publications32

  1. ncbi Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activities
    Philippe Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
    Mol Neurobiol 25:1-17. 2002
    ....
  2. ncbi Regulation by complement C3a and C5a anaphylatoxins of cytokine production in human umbilical vein endothelial cells
    Tiphaine Monsinjon
    Laboratory of Immunology, INSERM U519, IFRMP23, University of Rouen, France
    FASEB J 17:1003-14. 2003
    ..Finally, we showed that C3a and C5a both strongly activate downstream MAP kinase signaling pathways (p44 and p42 Erk kinases)...
  3. ncbi Molecular and cellular insights into the coxsackie-adenovirus receptor: role in cellular interactions in the stem cell niche
    Mathieu Hauwel
    Department of Medical Biochemistry and Immunology, Brain Inflammation and Immunity Group BIIG, Cardiff University, Heath Park, UK
    Brain Res Brain Res Rev 48:265-72. 2005
    ..Elucidating the other signalling molecules and manipulating the stromal-vascular niche for example by adenovirus gene therapy remain important goals for future clinical applications...
  4. ncbi Complement components of the innate immune system in health and disease in the CNS
    P Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
    Immunopharmacology 49:171-86. 2000
    ..Moreover, we discuss evidence suggesting that local C activation may contribute to tissue remodelling activities during repair in the CNS...
  5. ncbi Complement: a unique innate immune sensor for danger signals
    Philippe Gasque
    Brain Inflammation and Immunity Group BIIG, Department of Medical Biochemistry and Immunology, College of Medicine, University of Wales, Cardiff CF144XN, UK
    Mol Immunol 41:1089-98. 2004
    ....
  6. ncbi The receptor for complement anaphylatoxin C3a is expressed by myeloid cells and nonmyeloid cells in inflamed human central nervous system: analysis in multiple sclerosis and bacterial meningitis
    P Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, United Kingdom
    J Immunol 160:3543-54. 1998
    ..In multiple sclerosis, infiltrating lymphocytes did not express C3aR, but a strong staining was detected on smooth muscle cells (pericytes) surrounding blood vessels...
  7. pmc Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis
    S K Singhrao
    Department of Medical Biochemistry, Brain Inflammation and Immunity Group, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    Am J Pathol 157:905-18. 2000
    ..One reason for the susceptibility of neurons to complement-mediated damage in vivo may reside in their poor capacity to control complement activation...
  8. ncbi Endothelial cells, megakaryoblasts, platelets and alveolar epithelial cells express abundant levels of the mouse AA4 antigen, a C-type lectin-like receptor involved in homing activities and innate immune host defense
    Y D Dean
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, GB
    Eur J Immunol 31:1370-81. 2001
    ..g. uterus) were strongly stained for AA4. Although AA4 has been described on all hematopoietic progenitors, we found that only circulating immature B cells, monocytes and NK cells but not T cells and neutrophils expressed AA4...
  9. ncbi Role of complement in inflammation and injury in the nervous system
    B P Morgan
    University of Wales College of Medicine, Cardiff, UK
    Exp Clin Immunogenet 14:19-23. 1997
    ..The evidence suggests that C synthesis and activation in the brain are important in immune defence at this site but may also play a role in brain disease...
  10. ncbi Differential expression of individual complement regulators in the brain and choroid plexus
    S K Singhrao
    Department of Pathology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    Lab Invest 79:1247-59. 1999
    ..The demonstration herein that neurons express only very low levels of CD59 and MCP and lack both CR1 and DAF might explain their susceptibility to C damage...
  11. ncbi Innate immunity and brain inflammation: the key role of complement
    Karen Francis
    Department of Medical Biochemistry, Brain Inflammation and Immunity Group, University of Wales College of Medicine, Cardiff, CF14 4XN, UK
    Expert Rev Mol Med 5:1-19. 2003
    ..Knowledge of the unique molecular and cellular innate immunological interactions that occur in the development and resolution of pathology in the brain should facilitate the design of effective therapeutic strategies...
  12. ncbi Complement C3a receptors in the pituitary gland: a novel pathway by which an innate immune molecule releases hormones involved in the control of inflammation
    Karen Francis
    Brain Inflammation and Immunity Group, Department of Medical Biochemistry, University of Wales College of Medicine, Tenovus Bldg, Heath Park, Cardiff, CF14 4XN, UK
    FASEB J 17:2266-8. 2003
    ..We propose that the complement innate immune molecules (cytokines) modulate tissue-specific and systemic inflammatory responses through communication with the endocrine pituitary gland...
  13. ncbi Activation of complement in the central nervous system: roles in neurodegeneration and neuroprotection
    Johan van Beek
    Brain Inflammation and Immunity Group, Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Cardiff, UK
    Ann N Y Acad Sci 992:56-71. 2003
    ..Because many effects of the complement appear to promote neuronal survival and tissue remodeling, directing activation of the complement system in the brain may provide a better therapeutic rationale than inhibiting it...
  14. ncbi Human C1qRp is identical with CD93 and the mNI-11 antigen but does not bind C1q
    Eamon P McGreal
    Brain Inflammation and Immunity Group, Department of Medical Biochemistry, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, Wales, UK
    J Immunol 168:5222-32. 2002
    ..Collectively, these data indicate that C1qRp is not a receptor for C1q, and they support the emerging role of C1qRp (here renamed CD93) in functions relevant to intercellular adhesion...
  15. pmc Identification of an astrocyte cell population from human brain that expresses perforin, a cytotoxic protein implicated in immune defense
    P Gasque
    Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, CF4 4XX, United Kingdom
    J Exp Med 187:451-60. 1998
    ..These findings demonstrate that perforin expression is not unique to lymphoid cells and suggest that perforin produced by a subpopulation of astrocytes plays a role in inflammation in the brain...
  16. ncbi C3A binds to the seven transmembrane anaphylatoxin receptor expressed by epithelial cells and triggers the production of IL-8
    T Monsinjon
    Faculté Mixte de Médecine Pharmacie, INSERM U519, Rouen, France
    FEBS Lett 487:339-46. 2001
    ..Pre-treatment of ECV 304 with pertussis toxin inhibited IL-8 response induced by C3a, indicating that the action of C3a was mediated by a G protein coupled pathway...
  17. ncbi Molecular and cellular properties of the rat AA4 antigen, a C-type lectin-like receptor with structural homology to thrombomodulin
    Y D Dean
    Brain Inflammation and Immunity Group, Medical Biochemistry Department, University of Wales College of Medicine, Cardiff, CF144XN, United Kingdom
    J Biol Chem 275:34382-92. 2000
    ..As expected, the macrophage cell line NR8383 expressed weak levels of AA4. Taken together, our results support the idea that AA4/C1qRp is involved in some cell-cell interactions...
  18. ncbi Innate (inherent) control of brain infection, brain inflammation and brain repair: the role of microglia, astrocytes, "protective" glial stem cells and stromal ependymal cells
    Mathieu Hauwel
    Department of Medical Biochemistry and Immunology, Brain Inflammation and Immunity Group BIIG, University of Wales College of Medicine, Tenovus Building, Heath Park, Cardiff, UK
    Brain Res Brain Res Rev 48:220-33. 2005
    ..Understanding the mechanisms involved in the nurturing of damaged neurons by protective glial stem cells with the safe clearance of cell debris could lead to remedial strategies for chronic brain diseases...
  19. ncbi Decay-accelerating factor (CD55) is expressed by neurons in response to chronic but not acute autoimmune central nervous system inflammation associated with complement activation
    Johan van Beek
    Brain Inflammation Immunity Group BIIG, Cardiff University, Cardiff, United Kingdom
    J Immunol 174:2353-65. 2005
    ..We conclude that increased CD55 expression by neurons may represent a key protective signaling mechanism mobilized by brain cells to withstand complement activation and to survive within an inflammatory site...
  20. ncbi Innate immunity and protective neuroinflammation: new emphasis on the role of neuroimmune regulatory proteins
    M Griffiths
    Brain Inflammation and Immunity Group BIIG, Department of Medical Biochemistry, School of Medicine, Cardiff University, CF144XN Cardiff, United Kingdom
    Int Rev Neurobiol 82:29-55. 2007
    ..Moreover, NIRegs have direct beneficial effects on neurogenesis and contributing to brain tissue remodeling...
  21. ncbi Complement regulator loss on apoptotic neuronal cells causes increased complement activation and promotes both phagocytosis and cell lysis
    Duncan S Cole
    Department of Medical Biochemistry and Immunology, Wales College of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom
    Mol Immunol 43:1953-64. 2006
    ..The data suggest that therapeutic MMP inhibition, by restricting loss of CD46, may limit neuronal damage in neurological disease...
  22. ncbi CD46 plays a key role in tailoring innate immune recognition of apoptotic and necrotic cells
    Kristina Elward
    Brain Inflammation and Immunity Group BI2G, Department of Medical Biochemistry and Immunology, School of Medicine, Heath Park Campus, Cardiff University, Cardiff CF14 4XN, United Kingdom
    J Biol Chem 280:36342-54. 2005
    ....
  23. ncbi Immunoglobulin and cytokine expression in mixed lymphocyte cultures is reduced by disruption of gap junction intercellular communication
    E Oviedo-Orta
    University of Wales College of Medicine, Department of Medical Biochemistry, Wales Heart Research Institute, Heath Park, Cardiff CF14 4XN, Wales, U K
    FASEB J 15:768-74. 2001
    ..The results indicate that intercellular signaling across gap junctions is an important component of the mechanisms underlying metabolic cooperation in the immune system...
  24. ncbi Human endosialin (tumor endothelial marker 1) is abundantly expressed in highly malignant and invasive brain tumors
    Jennifer Brady
    Brain Inflammation and Immunity Group, Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    J Neuropathol Exp Neurol 63:1274-83. 2004
    ..Endosialin colocalized with thrombomodulin, suggesting the proteins may have complementary functions in tumor progression...
  25. ncbi "Eat me" and "don't eat me" signals govern the innate immune response and tissue repair in the CNS: emphasis on the critical role of the complement system
    Kristina Elward
    Brain Inflammation and Immunity Group BIIG, Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Cardiff CF144XN, Wales, UK
    Mol Immunol 40:85-94. 2003
    ..Further knowledge of the innate immune response in the CNS will greatly help to delineate the novel therapeutic routes to protect from CNS inflammation and neurodegeneration...
  26. ncbi C3d binding to the myelin oligodendrocyte glycoprotein results in an exacerbated experimental autoimmune encephalomyelitis
    Jean François Jégou
    INSERM U413, Institut Fédératif de Recherches Multidisciplinaires sur les Peptides 23, University of Rouen, Place Emile Blondel, Mont Saint Aignan Cedex, France
    J Immunol 178:3323-31. 2007
    ..These results suggest that binding of C3d to self-Ags could increase the severity of an autoimmune disease by enhancing the adaptive autoimmune response...
  27. doi Complement factor H, a marker of self protects against experimental autoimmune encephalomyelitis
    Mark R Griffiths
    Department of Medical Biochemistry, Cardiff University, United Kingdom
    J Immunol 182:4368-77. 2009
    ..Our data argue for a key regulatory activity of fH in neuroprotection and provide novel therapeutic avenues for CNS chronic inflammatory diseases...
  28. ncbi Receptors for the anaphylatoxins C3a and C5a are expressed in human atherosclerotic coronary plaques
    Riina Oksjoki
    Wihuri Research Institute, Kalliolinnantie 4, FIN 00140 Helsinki, Finland
    Atherosclerosis 195:90-9. 2007
    ....
  29. ncbi Presence of functional TLR2 and TLR4 on human adipocytes
    Sandrine Bes-Houtmann
    Laboratoire de Biochimie et de Génétique Moléculaire EA2526, Universite de la Reunion, Saint Denis, Ile de La Réunion, France
    Histochem Cell Biol 127:131-7. 2007
    ..Thus, it is clear that these receptors are functional in human adipocytes. This study adds weight to the argument that human fat tissue plays a potential role in innate immunity...
  30. ncbi High levels of complement C3a receptor in the glomeruli in lupus nephritis
    Masashi Mizuno
    Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan
    Am J Kidney Dis 49:598-606. 2007
    ....
  31. ncbi Neuroinvasion by pathogens: a key role of the complement system
    Cornelia Speth
    Institute of Hygiene and Social Medicine, University of Innsbruck and Ludwig Boltzmann Institute for AIDS Research, Fritz Pergl Str 3, A 6020 Innsbruck, Austria
    Mol Immunol 38:669-79. 2002
    ..The three main focuses are: (i) C activation and lysis of pathogens in the brain; (ii) C-dependent neuroinvasion mechanisms (iii) uncontrolled C activation in inflamed CNS contributing to tissue damage...
  32. ncbi Complement activation in human prion disease
    Gabor G Kovacs
    Institute of Neurology, University of Vienna, Vienna, Austria
    Neurobiol Dis 15:21-8. 2004
    ..The neuronal localization of the membrane attack complex correlates well with the severity of disease-specific pathology and TUNEL labeling of neurons, irrespective of genotype or molecular phenotype of human prion diseases...