Neuroinflammatory State of Multiple Sclerosis andStrategies for Biotherapeutics Development

Multiple Sclerosis (MS) is one of the most prevalent neurological disabilitiesin young adults. The pathogenesis of MS is characterized by demyelinationand neurodegeneration in the central nervous system (CNS) as the ruinousresult of chronic activation of the immune system. All clinical forms of MS,including relapsing-remitting multiple sclerosis (RRMS), secondaryprogressive multiple sclerosis (SPMS), and the primary progressive MS(PPMS), demonstrate inflammation as a common symptom. In variousautoimmune diseases like MS, the ability of the immune system to set abalance between pro-inflammatory and anti-inflammatory responses is lost.In this review, the imbalance between pro-inflammatory and antiinflammatoryresponses of immune cells and their role in MS progression isdiscussed. Disturbing the balance of Th۱/Th۲ and Th۱۷/Treg cells andM۱/M۲ phenotypes of macrophages and microglial plays a key role in thedevelopment and progression of MS. In this review, we first depict an outlineof regulatory immune cells in which the inflammatory-related genes are mosthighly expressed, and regulate differentiation and state of these cells. Second,we discuss shreds of evidence that confirm how B cells play both pathogenicand protective roles in MS disease. Third, we point out the pros and cons of Bcell/T cell-targeted therapies in clinical trials.

کلیدواژه ها:

Autoimmune disease ، Central nervous system ، Demyelination ، Immune cells ، Multiple sclerosis