Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease
- 31 May 2007
- journal article
- Published by Elsevier BV in Molecular Immunology
- Vol. 44 (12), 3132-3136
- https://doi.org/10.1016/j.molimm.2007.02.002
Abstract
No abstract availableKeywords
This publication has 21 references indexed in Scilit:
- T-cell regulation: with complements from innate immunityNature Reviews Immunology, 2006
- Complement and demyelinating disease: No MAC needed?Brain Research Reviews, 2006
- The role of the complement system in CNS inflammatory diseasesExpert Review of Clinical Immunology, 2006
- Expression of C5a in the brain does not exacerbate experimental autoimmune encephalomyelitisNeuroscience Letters, 2005
- Critical Requirement of CD11b (Mac-1) on T Cells and Accessory Cells for Development of Experimental Autoimmune EncephalomyelitisThe Journal of Immunology, 2005
- Blockade of the C5a receptor fails to protect against experimental autoimmune encephalomyelitis in ratsClinical and Experimental Immunology, 2004
- Complement C5 in Experimental Autoimmune Encephalomyelitis (EAE) Facilitates Remyelination and Prevents GliosisThe American Journal of Pathology, 2003
- Activation of Complement in the Central Nervous SystemAnnals of the New York Academy of Sciences, 2003
- Roles of the Complement System in Human Neurodegenerative DisordersMolecular Neurobiology, 2002
- Genetic variation among 129 substrains and its importance for targeted mutagenesis in miceNature Genetics, 1997