Abstract
Mesenchymal stem cells have been demonstrated to ameliorate experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, prompting clinical trials in multiple sclerosis which are currently ongoing. An important question is whether this therapeutic effect generalises to other autoimmune neurological diseases. We performed two trials of efficacy of MSCs in experimental autoimmune neuritis (EAN) in Lewis (LEW/Han MHsd) rats, a model of human autoimmune inflammatory neuropathies. No differences between the groups were found in clinical, histological or electrophysiological outcome measures. This was despite the ability of mesenchymal stem cells to inhibit proliferation of CD4+ T-cells in vitro. Therefore the efficacy of MSCs observed in autoimmune CNS demyelination models do not necessarily generalise to the treatment of other forms of neurological autoimmunity.
Highlights
Therapeutic efficacy of early administration of high dose of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been reported in the treatment of mouse experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS) [1,2]
Lewis rat-derived CD90+/CD452/CD11b2 mesenchymal stem cells grew in monolayer culture and their ability to inhibit T-cell proliferation was assessed by coculture with myelin-reactive CD4+ T-cells
We have shown that rat and human BM-MSCs, delivered intravenously at a similar time, do not lead to any discernable neurological, neurophysiological or histopathological improvement of experimental autoimmune neuritis (EAN) in Lewis rats, despite their mesenchymal potential and ability to inhibit T-cell proliferation in vitro
Summary
Therapeutic efficacy of early administration of high dose of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been reported in the treatment of mouse experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS) [1,2]. Previous studies suggested that these and other types of stem cells ameliorate autoimmune-mediated demyelination in the CNS through regulation of the inflammatory response [2,5]. These findings raise an important question as to whether BM-MSCs might be beneficial in other inflammatory demyelinating diseases, such as Guillain-Barresyndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). We tested whether intravenously delivered BM-MSCs were therapeutically beneficial in experimental autoimmune neuritis (EAN), an autoimmune peripheral neuropathy that has served as a model for GBS and CIDP [6,7]
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