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Commentary


           Meningeal inflammation and multiple sclerosis



           Li-Ping Liu
           Departments of Pain Management and Neurosciences, Lerner Research Institute and Anaesthesiology Institute, Cleveland Clinic,
           Cleveland, OH 44195, USA.









                                      Dr. Liu obtained her Ph.D. from Fudan University, Shanghai, China. She currently is a Project Scientist at
                                      the Cleveland Clinic, Cleveland, Ohio, USA. Dr. Liu has a record of remarkable publications in top impact
                                      journals such as Nature Neuroscience. She is an internationally recognized scientist with the expertise in
                                      the neuroinflammation and neurodegenerative diseases.










           Multiple sclerosis (MS) is a chronic inflammatory   between the encephalitogenic T helper 17 (Th17) cell
           demyelinating disease of the central nervous system   and lymphotoxin pathways contributes to the formation
           (CNS).  Inflammation  in  MS  is  characterized  by   of TLTs.
           infiltration of peripheral immune cells into the
           CNS, especially in the meninges. [1-4]  The infiltration   First, they made use of the SJL/J EAE model, which
           into meninges, which has been referred to as        mimics progressive MS, to investigate the location and
                                                                                        [7]
           tertiary lymphoid tissues (TLTs), is a likely first step   cellular composition of TLTs.  They found that T cells
           preceding infiltration into the CNS parenchyma.     were the initial population in meningeal TLTs, while B
           These invading autoreactive immune cells destroy    cells invaded the meninges later. Based on a previous
           myelin, the insulation surrounding neuronal axons,   report showing the importance of Th17 cells in promoting
           and cause demyelination in subpial and cortical     TLTs, [6,7]  they established an adoptively transferred
           areas, promoting disease pathogenesis. Experimental   encephalitogenic Th17 in the SJL/J EAE model. They
           autoimmune encephalomyelitis (EAE), a widely used   found that Th17 cells could rapidly populate, proliferate,
           murine model of MS, also shares this characteristic. [5,6]    and secrete cytokines in the meninges. The TLTs formed
           However, what cellular components and molecular     by Th17 cells and B cells were also associated with subpial
           pathways support infiltrating lymphocyte retention   and parenchyma demyelination, as shown by histological
           and production within the meninges as well as       staining.  Thus the authors have established a good
                                                                      [7]
           further invading into the CNS parenchyma are still   model (Th17 cells A/T model) for further investigation of
                                [7]
           not clear. Pikor  et al.  first reported that stromal   the cellular and molecular mechanisms of TLTs.
           cells in the inflamed CNS meninges (TLTs) play an
           important role in the neuroinflammatory process     What  are  the  roles  of  infiltrating  Th17  cells  in  the
           of MS. They also demonstrated that collaboration    remodeling of stromal cells in the meninges? They
                                                               found that 1 out of the 4 populations of stromal cells in
           Corresponding Author: Dr. Li-Ping Liu, Departments of Pain   meninges, meningeal FRC-like cells [a subpopulation
           Management and Neurosciences, Cleveland Clinic, 9500 Euclid
           Avenue/NE60, Cleveland, OH 44195, USA. Email: liul@ccf.org
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                                                                Cite this article as: Liu LP. Meningeal inflammation and multiple sclerosis.
                                    DOI: 10.20517/2347-8659.2016.22  Neuroimmunol Neuroinflammation 2016;3:145-6.
                                                                Received: 30-04-2016; Accepted: 09-05-2016




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