Abstract
Multiple sclerosis (MS) is a chronic autoimmune disease that affects the myelination of the neurons present in the central nervous system (CNS). The exact etiology of MS development is unclear, but various environmental and genetic factors might play a role in initiating the disease. Experimental autoimmune encephalomyelitis (EAE) is a mouse model that is used to study the pathophysiology of MS disease as well as the effects of possible therapeutic agents. In addition, autoreactive immune cells trigger an inflammatory process upon the recognition of CNS antigens, which leads to destruction of the neurons. These include innate immune cells such as macrophages, dendritic cells, and natural killer cells. Additionally, the activation and extravasation of adaptive immune cells such as CD4+ T cells into the CNS may lead to further exacerbation of the disease. However, many studies revealed that immune cells could have either a protective or pathological role in MS. In this review, we highlight the roles of innate and adaptive immune cellular and soluble players that contribute to the pathogenesis of MS and EAE, which may be used as potential targets for therapy.
Highlights
Multiple sclerosis (MS) is chronic autoimmune disabling diseases of the central nervous system (CNS) characterized by varying degrees of demyelination of uncertain etiology that is thought to be associated with specific environmental and genetic factors [1].The pathological characteristics of MS and its progression include an interplay between specific mechanisms mainly inflammation, which is thought to be the triggering point in the course of the disease, demyelination, axonal damage, and gliosis [2].Multiple sclerosis has four clinically defined subtypes, with relapsing-remitting multiple sclerosis (RRMS) being the most common
RRMS is distinguished by its stable course between the attacks, but this could shift to a progressive stage, which is known as secondaryprogressive multiple sclerosis (SPMS) [3]
Women who used vitamin D supplements had a 41% reduced risk of developing MS [68]. This was further supported by another study where subjects with serum levels of the circulating form of vitamin D3, 25-hydroxyvitamin D, greater than 100 nmol/L (40 ng/mL) had a 62% lower chance of developing MS [69]. These results suggest that a possible mechanism of action for these drugs is potentiating the cytolytic activity of NK cells against dendritic cells (DCs), which impede the latter from presenting autoantigens to autoreactive T cells
Summary
Multiple sclerosis (MS) is chronic autoimmune disabling diseases of the central nervous system (CNS) characterized by varying degrees of demyelination of uncertain etiology that is thought to be associated with specific environmental and genetic factors [1]. + T cells in the periphery, or stress by dendritic cells or macrophages and presented to CD4 such as inflammation, genetics, and some environmental factors cause damage to the myelin protein such as inflammation, genetics, and some environmental factors cause damage to the myelin proof the axons, releasing myelin antigens that bypass the blood–brain barrier (BBB) and induce an tein of the axons, releasing myelin antigens that bypass the blood–brain barrier (BBB) and induce autoimmune response in the periphery These events activate CD4+ T cells, which produce inflammatory cytokines and differentiate into Th1 that produce IFN-γ, or T helper 17 (Th17) cells producing interleukin 17 (IL-17) or interleukin 22 (IL-22), which permeabilize the BBB. Blood tests can be used to exclude the presence of viral and other infectious agents that may elicit neurological symptoms similar to those observed in MS patients [15,16]
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