Abstract
[This corrects the article DOI: 10.1371/journal.pone.0057820.].
Highlights
Progressive multiple sclerosis (MS) is characterized by steady progression of neurological disability without remission
Analysis of Th1- and Th17-phenotypes showed that SPMS and PPMS patients had an increased frequency of IL23-receptor (IL23R)+CD4+T-cells, presumably Th17-cells [35], in blood compared to healthy controls (HC) (Figure 1H–I)
Previous studies have indicated the presence of systemic and intrathecal inflammation in progressive MS, but it is unclear to what extent systemic inflammation mirrors intrathecal inflammation and whether systemic inflammation contributes to intrathecal inflammation and disease progression
Summary
Progressive multiple sclerosis (MS) is characterized by steady progression of neurological disability without remission. A low rate of relapses and gadolinium-enhancing lesions, pronounced atrophy and limited efficacy of treatment has supported a view where axonal loss independent of inflammation is thought to be the substrate for disease progression [4]. This view was challenged by recent pathology studies, which indicate that in progressive MS CNS inflammation is abundant and correlates with axonal damage and disease progression [5,6]. ELFs are associated with more rapid disease progression, cortical lesions, meningeal and white matter inflammation, atrophy and neuronal loss [9,10]. Monocytes and dendritic cells have been implicated in MS immunopathology [12,13,14]
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