Abstract
Multiple sclerosis, the clinical features and pathological correlate for which were first described by Charcot, is a chronic neuroinflammatory disease with unknown etiology and variable clinical evolution. Although neuroinflammation is a descriptive denominator in multiple sclerosis based on histopathological observations, namely the penetration of leukocytes into the central nervous system, the clinical symptoms of relapses, remissions and progressive paralysis are the result of losses of myelin and neurons. In the absence of etiological factors as targets for prevention and therapy, the definition of molecular mechanisms that form the basis of inflammation, demyelination and toxicity for neurons have led to a number of treatments that slow down disease progression in specific patient cohorts, but that do not cure the disease. Current therapies are directed to block the immune processes, both innate and adaptive, that are associated with multiple sclerosis. In this review, we analyze the role of cytokines in the multiple sclerosis pathogenesis and current/future use of them in treatments of multiple sclerosis.
Highlights
Multiple sclerosis (MS), the clinical features and pathological correlate for which were first described by Charcot, is a chronic neuroinflammatory disease with unknown etiology and variable clinical evolution
IL17-producing T cells were dramatically reduced in the central nervous system (CNS) of IL-23p19-deficient mice. These results suggested that IL-17-producing CD4+ T cells are a distinct and novel Th subset that exacerbates autoimmunity, and designated them Th17 cells [41,42]
No increase in the numbers and expression of IL-17 mRNA by mononuclear cells isolated from the cerebrospinal fluid (CSF) was observed in MS patients, but higher levels of IL-17 mRNA were observed in the CSF than in the blood, with the highest levels in the blood detected during clinical exacerbations [52]
Summary
Multiple sclerosis (MS), the clinical features and pathological correlate for which were first described by Charcot, is a chronic neuroinflammatory disease with unknown etiology and variable clinical evolution. With the latest tools of molecular biology, such as whole genome sequencing, genome-wide association studies [10,11], gene expression profiling coupled with protein analysis [12,13], we may be able, in the future, to define common identifiers for specific cohorts of MS patients, to perform better and earlier diagnoses and, hopefully, discover etiological factors. This is presently not yet possible and therapies are directed to block the immune processes, both innate and adaptive, that are associated with MS. In this review we analyze the role of cytokines in the MS pathogenesis and current/future use of them in treatments of multiple sclerosis
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