Multiple sclerosis is a demyelinating disease of the central nervous system of an inflammatory, chronic and progressive nature. The destruction of the myelin sheath and axonal degeneration results in scattered lesions in the central nervous system, especially in the optic nerves, brainstem, spinal cord and periventricular white matter. The dissemination of these lesions results in neurological deficits of variable course (208). The infiltration of activated T lymphocytes and the secretion of inflammatory mediators by these cells results in endothelial changes in the blood-brain barrier and stimulate the inflammatory cascade (209). The production of IFN-γ by activated TH1 lymphocytes activates macrophages that secrete proteases and TNF-α, which contribute to the destruction of oligodendrocytes. The activation of macrophages by IFN-γ also results in the production of high levels of nitric oxide. This increase in nitric oxide inhibits mitochondrial respiration and reduces the synthesis of ATP, leading to the axonal injury observed in the pathological process of the disease (210). Regarding the studies in which hMSCs were used for the treatment of multiple sclerosis (102, 121–145, 154), five studies (125, 131, 132, 134, 135) were conducted in humans, 19 (102, 121–124, 126–129, 133, 136–139, 141, 143–145, 154) were conducted in mice and three studies (130, 140, 142) used rats as the experimental model. Among these studies, 16 used hMSCs isolated from the bone marrow (102, 122, 123, 125–128, 131–137, 138, 143, 154), seven isolated hMSCs from the adipose tissue (121, 128, 130, 136, 140, 141, 145), four isolated hMSCs from the umbilical cord (124, 128, 142, 144) and two isolated hMSCs from the placenta (129, 139). In only one study (102), hMSCs were obtained from the differentiation of embryonic stem cells.