This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
8. References
W. F. Hickey, Leukocyte traffic in the central nervous system: the participants and their roles, Semin Immunol 11(2), 125–137 (1999).
C. Lucchinetti, W. Bruck, J. Parisi, B. Scheithauer, M. Rodriguez, and H. Lassmann, Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination, Ann Neurol 47(6), 707–717 (2000).
G. Fazekas and T. Tabira, What transgenic and knockout mouse models teach us about experimental autoimmune encephalomyelitis, Rev Immunogenet 2(1), 115–132 (2000).
P. F. Stahel, D. Nadal, H. W. Pfister, P. M. Paradisis, and S. R. Barnum, Complement C3 and factor B cerebrospinal fluid concentrations in bacterial and aseptic meningitis, Lancet 349(9069), 1886–1887 (1997).
B. P. Morgan and P. Gasque, Expression of complement in the brain: role in health and disease, Immunol Today 17(10), 461–466 (1996).
P. A. Andrews, J. E. Finn, C. M. Lloyd, W. Zhou, P. W. Mathieson, and S. H. Sacks, Expression and tissue localization of donor-specific complement C3 synthesized in human renal allografts, Eur J Immunol 25(4), 1087–1093 (1995).
J. R. Pratt, S. A. Basheer, and S. H. Sacks, Local synthesis of complement component C3 regulates acute renal transplant rejection, Nat Med 8(6), 582–587 (2002).
M. E. Sanders, C. L. Koski, D. Robbins, M. L. Shin, M. M. Frank, and K. A. Joiner, Activated terminal complement in cerebrospinal fluid in Guillain-Barre syndrome and multiple sclerosis, J Immunol 136(12), 4456–4459 (1986).
J. C. Cyong, S. S. Witkin, B. Rieger, E. Barbarese, R. A. Good, and N. K. Day, Antibody-independent complement activation by myelin via the classical complement pathway, J Exp Med 155(2), 587–598 (1982).
P. Vanguri, C. L. Koski, B. Silverman, and M. L. Shin, Complement activation by isolated myelin: activation of the classical pathway in the absence of myelin-specific antibodies, Proc Natl Acad Sci USA 79(10), 3290–3294 (1982).
C. L. Koski, P. Vanguri, and M. L. Shin, Activation of the alternative pathway of complement by human peripheral nerve myelin, J Immunol 134(3), 1810–1814 (1985).
S. K. Singhrao, J. W. Neal, N. K. Rushmere, B. P. Morgan, and P. Gasque, Spontaneous classical pathway activation and deficiency of membrane regulators render human neurons susceptible to complement lysis, Am J Pathol 157(3), 905–918 (2000).
C. Linington, B. P. Morgan, N. J. Scolding, P. Wilkins, S. Piddlesden, and D. A. Compston, The role of complement in the pathogenesis of experimental allergic encephalomyelitis, Brain 112(Pt 4), 895–911 (1989).
K. Kerekes, J. Prechl, Z. Bajtay, M. Jozsi, and A. Erdei, A further link between innate and adaptive immunity: C3 deposition on antigen-presenting cells enhances the proliferation of antigen-specific T cells, Int Immunol 10(12), 1923–1930 (1998).
B. Dietzschold, W. Schwaeble, M. K. Schafer, D. C. Hooper, Y. M. Zehng, F. Petry, H. Sheng, T. Fink, M. Loos, H. Koprowski, and., Expression of C1q, a subcomponent of the rat complement system, is dramatically enhanced in brains of rats with either Borna disease or experimental allergic encephalomyelitis, J Neurol Sci 130(1), 11–16 (1995).
T. G. Johns and C. C. Bernard, Binding of complement component Clq to myelin oligodendrocyte glycoprotein: a novel mechanism for regulating CNS inflammation, Mol Immunol 34(1), 33–38 (1997).
D. M. Calida, C. Constantinescu, E. Purev, G. X. Zhang, E. S. Ventura, E. Lavi, and A. Rostami, Cutting edge: C3, a key component of complement activation, is not required for the development of myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalomyelitis in mice, J Immunol 166(2), 723–726 (2001).
S. Nataf, S. L. Carroll, R. A. Wetsel, A. J. Szalai, and S. R. Barnum, Attenuation of experimental autoimmune demyelination in complement-deficient mice, J Immunol 165(10), 5867–5873 (2000).
L. J. van der Laan, S. R. Ruuls, K. S. Weber, I. J. Lodder, E. A. Dopp, and C. D. Dijkstra, Macrophage phagocytosis of myelin in vitro determined by flow cytometry: phagocytosis is mediated by CR3 and induces production of tumor necrosis factor-alpha and nitric oxide, J Neuroimmunol 70(2), 145–152 (1996).
F. Reichert and S. Rotshenker, Complement-receptor-3 and scavenger-receptor-AI/II mediated myelin phagocytosis in microglia and macrophages, Neurobiol Dis 12(1), 65–72 (2003).
L. A. Boos, A. J. Szalai, and S. R. Barnum, Murine complement C4 is not required for experimental autoimmune encephalomyelitis, Glia 49(1), 158–160 (2005).
S. H. Weerth, H. Rus, M. L. Shin, and C. S. Raine, Complement C5 in experimental autoimmune encephalomyelitis (EAE) facilitates remyelination and prevents gliosis, Am J Pathol 163(3), 1069–1080 (2003).
G. T. Tran, S. J. Hodgkinson, N. Carter, M. Killingsworth, S. T. Spicer, and B. M. Hall, Attenuation of experimental allergic encephalomyelitis in complement component 6-deficient rats is associated with reduced complement C9 deposition, Pselectin expression, and cellular infiltrate in spinal cords, J Immunol 168(9), 4293–4300 (2002).
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2006 Springer Science+Business Media, LLC
About this paper
Cite this paper
Terényi, N., Prechl, J., Erdei, A. (2006). The Role of the Complement System in the Pathogenesis of Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis. In: Lambris, J.D. (eds) Current Topics in Complement. Advances in Experimental Medicine and Biology, vol 586. Springer, Boston, MA. https://doi.org/10.1007/0-387-34134-X_12
Download citation
DOI: https://doi.org/10.1007/0-387-34134-X_12
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-32231-5
Online ISBN: 978-0-387-34134-7
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)