EAE was induced in 14 marmosets by immunization with proteins from human myelin. At 21 days after immunization, B-cell depletion was achieved by weekly intravenous injections of a human-anti-human CD20 antibody that cross-reacts with marmoset CD20. MRI showed widespread brain white matter demyelination in control marmosets that was absent in CD20 antibody-treated marmosets. High-contrast postmortem MRI showed white matter lesions in 4 of the 7 antibody-treated marmosets, but these were significantly smaller than those in controls. The same technique revealed gray matter lesions in 5 control marmosets, but none in antibody-treated marmosets. Detailed analysis confirmed that inflammation, demyelination, and axonal damage were substantially reduced in brain, spinal cord, and optic nerves of CD20 antibody-treated marmosets.
Conclusion: B-cell depletion profoundly reduced the development of both white and gray matter lesions in the marmoset CNS. These data underline the central role of B cells in CNS inflammatory-demyelinating disease.
"I am not sure about the ethics of this study as anti-CD20 treatment has already been shown to be effective in MS and is in late stage development in phase 3 in both relapsing-remitting and primary progressive MS. Do you we need to do trials in primates at this stage? What do you think?"
Trials of anti-CD20 in MS: