Multiple sclerosis (MS) is an autoimmune disease with uncertain
aetiology. In this work, we used two genetically modified mice, each derived by
gene ablation to complement protein C5aR1 and C5L2 receptors, designed to
investigate their roles in mediating the disease model experimental autoimmune
encephalomyelitis (EAE). MR spectroscopy and DTI were measured using a 9.4T MRI
with cryoprobe at the level of lumbar spinal cord. Changes in metabolites and DTI
parameters indicate that the ablation of C5L2, to a greater extent than the ablation of C5aR1,
made these mice less susceptible to EAE induced neuronal damage compared to
wild-type mice.
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