Multiple sclerosis (MS) is an inflammatory disease of the centre nervous system (CNS) and is mediated by pathogenic autoreactive T cells, which trigger local inflammation and neuronal damage. Experimental allergic encephalomyelitis (EAE) is a model of MS. Currently, there is no effective therapies for MS. Human placental mesenchymal stem cells (MSCs) possess an immune suppressive property and can differentiate into neuronal cells, and therefore pMSCs may reduce neuronal damage in MS and its EAE model by suppressing the functions of T cell mediating inflammation and neuronal damage and/or replacing defective or damaged neurons. In this study, we are using human pMSCs in an EAE mice model to examine their efficiency in attenuating the encephalitogenic manifestation of the disease by modulating the neuroinflammatory process as a result of suppressing the functions of encephalitogenic T cells.
Immunomodulation properties of MSCs on immune cells including T cells, NK cells, B cells, monocyte and dendritic cells (DCs) (Abumaree et al., 2012)
Mesenchymal stem cells can induce neuron recovery in multiple sclerosis via a mechanism that stimulates oligodendrogenesis and decreases the numbers of Th1 and Th17 cells and their secretion of inflammatory cytokines while increasing the numbers of Th2 and Treg cells and their secretion of anti-inflammatory cytokines (Al Jumah and Abumaree, 2012).