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Regulation of neuroinflammatory properties of glial cells by T cell effector molecules

Neural Regeneration Research 2018年第2期13卷 234-236页

作者： chittappen k.prajeeth jochen huehn martin stangel clinical neuroimmunology and neurochemistry department of neurologyhannover medical schoolHannoverGermany experimental immunology helmholtz centre for infection researchBraunschweigGermany center of systems neuroscience hannover medical schoolGermany

Multiple sclerosis （MS） is a chronic inflammatory and neurodegenerative disorder that is thought to be mediated by autoreactive T lymphocytes that find their way into the central nervous system （CNS）. The pathological mechanism of MS is still being elucidated but it involves complex interactions between infiltrating immune cells and resi- dent glial cells within the CNS that culminate into strong neuroinflammation and axonal damage.

关键词： Regulation of neuroinflammatory properties of glial cells by T cell effector molecules Th CNS

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Mesenchymal stem cells require the peripheral immune system for immunomodulating effects in animal models of multiple sclerosis

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Neural Regeneration Research 2016年第1期11卷 90-91页

作者： Laura Salinas Tejedor Thomas Skripuletz martin stangel Viktoria Gudi Clinical Neuroimmunology and Neurochemistry Department of NeurologyHannover Medical SchoolHanoverGermany Center for Systems Neuroscience HannoverGermany

Multiple sclerosis（MS）is a chronic inflammatory disease of the central nervous system（CNS）that affects oligodendrocytes and myelin.Loss of myelin leads to progressive axonal damage and neuronal death resulting in neurodenegeration and functional disability.Several inflammatory factors influence the development of this neurological disorder.

关键词： disability migrate myelin axonal neuronal neurological progressive affects interleukin amyotrophic

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The choline pathway as a strategy to promote central nervous system(CNS) remyelination

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Neural Regeneration Research 2015年第9期10卷 1369-1370页

作者： Thomas Skripuletz Ralf A.Linker martin stangel Department of Neurology Hannover Medical School Department of Neurology University Hospital Erlangen Center for Systems Neuroscience

Multiple sclerosis is a chronic companied by demyelination inflammatory disease that is ac- and axonal damage resulting in neurological deficits. Remyelination is the natural endogenous repair mechanism of demyelinated axons and it is supposed to protect axons/neurons from degeneration and thus the patient from progressive disability （Franklin and Ffrench-Constant, 2008）. Current therapeutics for patients with multiple sclerosis are to some extent very effective in inhibiting neuroinflamma- tion and demyelination. However, to date there are no substanc- es available that can enhance remyelination. Remyelination is the result of recruitment/proliferation of new oligodendrocyte precursor cells （OPC） and differentiation into mature myelin producing oligodendrocytes （Franklin and Ffrench-Constant, 2008）. These processes are supported by many factors and signals and failure at any stage might lead to repair failure. Strategies to enhance myelin repair are either the promotion of endogenous repair mechanisms via modulation of OPC prolif- eration and oligodendrocyte differentiation or the transplantion of myelinating cells into lesions. Due to the multiloculated pro- cess in multiple sclerosis and the ethical problems with the cell source, the latter is less favoured. The endogenous promotion of remvelination could be achieved by several approaches such as：

关键词： CDP remyelination The choline pathway as a strategy to promote central nervous system OPC CNS

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