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      Human bone marrow-derived mesenchymal stem cells induce Th2-polarized immune response and promote endogenous repair in animal models of multiple sclerosis.

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          Abstract

          Cell-based therapies are attractive approaches to promote myelin repair. Recent studies demonstrated a reduction in disease burden in mice with experimental allergic encephalomyelitis (EAE) treated with mouse mesenchymal stem cells (MSCs). Here, we demonstrated human bone marrow-derived MSCs (BM-hMSCs) promote functional recovery in both chronic and relapsing-remitting models of mouse EAE, traced their migration into the injured CNS and assayed their ability to modulate disease progression and the host immune response. Injected BM-hMSCs accumulated in the CNS, reduced the extent of damage and increased oligodendrocyte lineage cells in lesion areas. The increase in oligodendrocytes in lesions may reflect BM-hMSC-induced changes in neural fate determination, since neurospheres from treated animals gave rise to more oligodendrocytes and less astrocytes than nontreated neurospheres. Host immune responses were also influenced by BM-hMSCs. Inflammatory T-cells including interferon gamma producing Th1 cells and IL-17 producing Th17 inflammatory cells and their associated cytokines were reduced along with concomitant increases in IL-4 producing Th2 cells and anti-inflammatory cytokines. Together, these data suggest that the BM-hMSCs represent a viable option for therapeutic approaches.

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          Author and article information

          Journal
          Glia
          Glia
          Wiley
          1098-1136
          0894-1491
          Aug 15 2009
          : 57
          : 11
          Affiliations
          [1 ] Case Western Reserve University, Centers for Stem Cells and Regenerative Medicine, Translational Neuroscience, Department of Neurosciences, Case School of Medicine, Cleveland, Ohio 44106, USA.
          Article
          NIHMS94902
          10.1002/glia.20841
          2706928
          19191336
          dbccf0a6-fbda-42de-83bb-0f6349c2c36c
          History

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