Abstract
Multiple sclerosis (MS) is a chronic, autoimmune, inflammatory demyelinating disorder of the central nervous system that leads to permanent neurological deficits. Current MS treatment regimens are insufficient to treat the irreversible neurological disabilities. Tremendous progress in the experimental and clinical applications of cell-based therapies has recognized stem cells as potential candidates for regenerative therapy for many neurodegenerative disorders including MS. Mesenchymal stem cells (MSC) and induced pluripotent stem cell (iPSCs) derived precursor cells can modulate the autoimmune response in the central nervous system (CNS) and promote endogenous remyelination and repair process in animal models. This review highlights studies involving the immunomodulatory and regenerative effects of mesenchymal stem cells and iPSCs derived cells in animal models, and their translation into immunomodulatory and neuroregenerative treatment strategies for MS.
Highlights
Multiple sclerosis (MS) is a chronic autoimmune, inflammatory, demyelinating, neurodegenerative disease of the central nervous system (CNS) of unknown etiology
There were no significant differences in these beneficial effects between EAE-Bone marrow (BM)-Mesenchymal stem cells (MSC) and MSCs obtained from wild-type syngeneic donors
Since MSCs could impact the fate of surrounding cells and microenvironments via cell-cell contact and soluble factors, the question whether the inflammatory microenvironment and cytokines secreted by inflammatory cells or other cells localized within the CNS exert influence on the biological properties of MSCs and therapeutic effects of transplanted cells is of great importance for further study
Summary
Multiple sclerosis (MS) is a chronic autoimmune, inflammatory, demyelinating, neurodegenerative disease of the central nervous system (CNS) of unknown etiology. In the acute phase, activated mononuclear cells, including lymphocytes, microglia, and macrophages destroy myelin and to a variable degree, oligodendrocytes. The endogenous oligodendrocyte precursor cells (OPCs) proliferate robustly in response to demyelination, but fail to differentiate terminally, resulting in failure of remyelination. This is associated with axonal transection leading to permanent neurological deficits. The permanent neuronal loss that starts early and characterizes the progressive stage of MS remains untreatable. Therapeutic options such as Mitoxantrone for PPMS patients are limited to symptomatic treatments and the long-term prognosis is generally poor [10]. Future therapeutic strategies are aimed to achieve neuroprotection, remyelination and regeneration of new oligodendrocytes and neurons [11]
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