Attenuation of Experimental Autoimmune Encephalomyelitis in a Common Marmoset Model by Dendritic Cell-Modulating Anti-ICAM-1 Antibody, MD-3.
Soon-Tae LeeSeung Pyo ParkHi-Jung ParkJoan R WicksJae-Il LeeYoung Ho SuhKyeong Cheon JungPublished in: Molecular neurobiology (2018)
MD-3 is a novel anti-human ICAM-1 monoclonal antibody that induces T cell tolerance in humanized mice via modulation of dendritic cell differentiation and efficiently suppresses the development of collagen-induced arthritis. This effect has also been observed in xenograft rejection in nonhuman primates, where grafts survived for more than 2.5 years following MD-3 administration. Here, we show that MD-3 can attenuate experimental autoimmune encephalomyelitis (EAE) that was induced in common marmoset monkeys by immunization with human myelin oligodendrocyte glycoproteins. MD-3 administration was initiated 1 week after immunization and efficiently delayed the development of EAE phenotypes, although the disease was not completely prevented. Based on the results of histopathological examination, MD-3 treatment greatly suppressed total inflammation with respect to demyelination, as well as T cell and microglial infiltration in the brain. However, the antibody response against myelin oligodendrocyte glycoprotein was not suppressed with this treatment protocol. These observations suggest that the MD-3 antibody has beneficial effects on the treatment of EAE via the suppression of T cell-mediated cellular responses.
Keyphrases
- molecular dynamics
- monoclonal antibody
- endothelial cells
- dendritic cells
- rheumatoid arthritis
- high glucose
- randomized controlled trial
- signaling pathway
- oxidative stress
- white matter
- clinical trial
- type diabetes
- neuropathic pain
- lipopolysaccharide induced
- multiple sclerosis
- spinal cord injury
- drug induced
- study protocol
- pluripotent stem cells
- subarachnoid hemorrhage
- cerebral ischemia