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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Baas, Frank Ramaglia, Valeria Hughes, Timothy R. Huitinga, Inge Wu, Xiaobo Morgan, B. Paul Donev, Rossen M. Ruseva, Marieta M. Neal, James W. |
| Description | Author Affiliation: Ramaglia V ( Department of Infection, Immunity, and Biochemistry, School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom. v.ramaglia@amc.nl); |
| Abstract | Microglial priming predisposes the brain to neurodegeneration and affects disease progression. The signal to switch from the quiescent to the primed state is unknown. We show that deleting the C3 convertase regulator complement receptor 1-related protein y (Crry) induces microglial priming. Mice that were double-knockout for Crry and either C3 or factor B did not show priming, demonstrating dependence on alternative pathway activation. Colocalization of C3b/iC3b and CR3 implicated the CR3/iC3b interaction in priming. Systemic lipopolysaccharide challenge overactivated primed microglia with florid expression of proinflammatory molecules, which were blocked by complement inhibition. Relevance for neurodegenerative disease is exemplified by human multiple sclerosis (MS) and by experimental autoimmune encephalomyelitis (EAE), a model of MS. In human MS, microglial priming was evident in perilesional white matter, in close proximity to C3b/iC3b deposits. EAE was accelerated and exacerbated in Crry-deficient mice, and was dependent on C activation. In summary, C3-dependent microglial priming confers susceptibility to other challenges. Our observations are relevant to progression in MS and other neurological diseases exacerbated by acute insults. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 3 |
| Volume Number | 109 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2012-02-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Complement C3 Immunology Cross-Priming Microglia Pathology Multiple Sclerosis Animals Cell Shape Complement C3b Complement Pathway, Alternative Encephalomyelitis, Autoimmune, Experimental Inflammation Inflammation Mediators Metabolism Lipopolysaccharides Administration & Dosage Pharmacology Mice Mice, Inbred C57BL Models, Immunological Receptors, Complement Deficiency Spinal Cord Up-Regulation Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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