Hundgeburth LC, Wunsch M, Rovituso D, Recks MS, Addicks K, Lehmann PV, Kuerten S (2013)
Publication Type: Journal article
Publication year: 2013
Book Volume: 146
Pages Range: 155-164
Journal Issue: 3
DOI: 10.1016/j.clim.2012.12.007
So far, studies of the human autoimmune disease multiple sclerosis (MS) have largely been hampered by the absence of a pathogenic B cell component in its animal model, experimental autoimmune encephalomyelitis (EAE). To overcome this shortcoming, we have previously introduced the myelin basic protein (MBP)-proteolipid protein (PLP) MP4-induced EAE, which is B cell and autoantibody-dependent. Here we show that MP4-immunized wild-type C57BL/6 mice displayed a significantly lower disease incidence when their complement system was transiently depleted by a single injection of cobra venom factor (CVF) prior to immunization. Considering the underlying pathomechanism, our data suggest that the complement system is crucial for MP4-specific antibodies to trigger CNS pathology. Demyelinated lesions in the CNS were colocalized with complement depositions. In addition, B cell deficient J
APA:
Hundgeburth, L.C., Wunsch, M., Rovituso, D., Recks, M.S., Addicks, K., Lehmann, P.V., & Kuerten, S. (2013). The complement system contributes to the pathology of experimental autoimmune encephalomyelitis by triggering demyelination and modifying the antigen-specific T and B cell response. Clinical Immunology, 146(3), 155-164. https://doi.org/10.1016/j.clim.2012.12.007
MLA:
Hundgeburth, Lorenz C., et al. "The complement system contributes to the pathology of experimental autoimmune encephalomyelitis by triggering demyelination and modifying the antigen-specific T and B cell response." Clinical Immunology 146.3 (2013): 155-164.
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