Affiliation: Cardiff University
- Human C1qRp is identical with CD93 and the mNI-11 antigen but does not bind C1qEamon 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...
- Complement C3a receptors in the pituitary gland: a novel pathway by which an innate immune molecule releases hormones involved in the control of inflammationKaren 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...
- Innate immunity and brain inflammation: the key role of complementKaren 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...
- Complement regulator loss on apoptotic neuronal cells causes increased complement activation and promotes both phagocytosis and cell lysisDuncan 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...
- Human endosialin (tumor endothelial marker 1) is abundantly expressed in highly malignant and invasive brain tumorsJennifer 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...
- Activation of complement in the central nervous system: roles in neurodegeneration and neuroprotectionJohan 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...
- Molecular and cellular insights into the coxsackie-adenovirus receptor: role in cellular interactions in the stem cell nicheMathieu 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...
- Innate (inherent) control of brain infection, brain inflammation and brain repair: the role of microglia, astrocytes, "protective" glial stem cells and stromal ependymal cellsMathieu 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...
- Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activitiesPhilippe Gasque
Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
Mol Neurobiol 25:1-17. 2002....
- Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitisCecile Canova
Brain Inflammation and Immunity Group, Department of Medical Biochemistry, Cardiff University, Heath Park, Cardiff, CF14 4XN, UK
J Neuroinflammation 3:22. 2006..However, epithelial cells of either the ependymal layer, one of the established niche for adult neural stem cells, or of the choroid plexus may be extremely vulnerable to bystander attack by cytotoxic and cytolytic complement components...
- "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 systemKristina 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...
- Regulation by complement C3a and C5a anaphylatoxins of cytokine production in human umbilical vein endothelial cellsTiphaine 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)...
- High levels of complement C3a receptor in the glomeruli in lupus nephritisMasashi Mizuno
Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan
Am J Kidney Dis 49:598-606. 2007....
- Receptors for the anaphylatoxins C3a and C5a are expressed in human atherosclerotic coronary plaquesRiina Oksjoki
Wihuri Research Institute, Kalliolinnantie 4, FIN 00140 Helsinki, Finland
Atherosclerosis 195:90-9. 2007....
- Complement: a unique innate immune sensor for danger signalsPhilippe 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....
- CD46 plays a key role in tailoring innate immune recognition of apoptotic and necrotic cellsKristina 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....
- Complement activation in human prion diseaseGabor 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...
- Decay-accelerating factor (CD55) is expressed by neurons in response to chronic but not acute autoimmune central nervous system inflammation associated with complement activationJohan 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...
- Protective DNA vaccination against myelin oligodendrocyte glycoprotein is overcome by C3d in experimental autoimmune encephalomyelitisJean François Jégou
INSERM U413, IFRMP 23, Laboratory of Cellular and Molecular Neuroendocrinology, University of Rouen, 76821 Mont Saint Aignan, France
Mol Immunol 44:3691-701. 2007..These findings suggest that C3d might be involved in self-tolerance breakdown and could contribute to the pathogenesis of central nervous system autoimmune disorders...