TY - BOOK ID - 135119468 TI - Cellular and Molecular Mechanisms in Pathogenesis of Multiple Sclerosis PY - 2020 PB - Basel, Switzerland MDPI - Multidisciplinary Digital Publishing Institute DB - UniCat KW - neutrophils KW - lymphocytes KW - NLR KW - multiple sclerosis KW - disease activity KW - inside-out KW - outside-in KW - oligodendrocytosis KW - demyelination KW - gliosis KW - histology KW - top-down proteomics KW - bioinformatics KW - mitochondria KW - CD4+ T cells KW - memory T cells KW - autoimmune disease KW - effector memory T cell KW - central memory T cell KW - tissue-resident T cell KW - experimental autoimmune encephalomyelitis KW - monocytes KW - granulocyte-macrophage colony-stimulating factor KW - S100B KW - relapsing–remitting experimental autoimmune encephalomyelitis KW - pentamidine KW - NG2-glia KW - progenitors KW - lineage KW - in utero electroporation KW - morphometric analyses KW - clonal analyses KW - lesioned brain KW - sphingosine-1-phosphate receptors KW - glutamate synaptic dysfunction KW - microglia KW - T lymphocytes KW - experimental autoimmune encephalomyelitis (EAE) KW - pro-inflammatory cytokines KW - neuroinflammation KW - ozanimod KW - AUY954 KW - A971432 KW - S1P1 KW - S1P5 KW - kynurenine pathway KW - kynurenic acid KW - oxidative stress KW - quinolinic acid KW - N-acetylserotonin KW - IDO KW - NAD+, multiple sclerosis KW - laquinimod KW - n/a KW - relapsing-remitting experimental autoimmune encephalomyelitis UR - https://www.unicat.be/uniCat?func=search&query=sysid:135119468 AB - Multiple sclerosis (MS) is one of the most common neurological disorders in young adults. The etiology of MS is not known, but it is generally accepted that it is autoimmune in nature. Our knowledge of the pathogenesis of MS has increased tremendously in the past decade through clinical studies and the use of experimental autoimmune encephalomyelitis (EAE), a model that has been widely used for MS research. Major advances in the field, such as understanding the roles of pathogenic Th17 cells, myeloid cells, and B cells in MS/EAE, as well as cytokine and chemokine signaling that controls neuroinflammation, have led to the development of potential and clinically approved disease-modifying agents (DMAs). There are many aspects related to the initiation, relapse and remission, and progression of MS that are yet to be elucidated. For instance, what are the genetic and environmental risk factors that promote the initiation of MS, and how do these factors impact the immune system? What factors drive the progression of MS, and what are the roles of peripheral immune cells in disease progression? How do the CNS-infiltrated immune cells interact with the CNS-resident glial cells when the disease progresses? What is the role of microbiome in MS? Can we develop animal models that better represent subcategories of MS? Understanding the cellular and molecular mechanisms that govern the pathogenesis of MS will help to develop novel and more specific therapeutic strategies that will ultimately improve clinical outcomes of the treatments. This Special Issue of Cells has published original research articles, a retrospective clinical report, and review articles that investigate the cellular and molecular basis of MS. ER -