The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis - PubMed (original) (raw)

Review

The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis

Samuel S Duffy et al. Mult Scler Int. 2014.

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterised by widespread areas of focal demyelination. Its aetiology and pathogenesis remain unclear despite substantial insights gained through studies of animal models, most notably experimental autoimmune encephalomyelitis (EAE). MS is widely believed to be immune-mediated and pathologically attributable to myelin-specific autoreactive CD4+ T cells. In recent years, MS research has expanded beyond its focus on CD4+ T cells to recognise the contributions of multiple immune and glial cell types to the development, progression, and amelioration of the disease. This review summarises evidence of T and B lymphocyte, natural killer cell, macrophage/microglial, astrocytic, and oligodendroglial involvement in both EAE and MS and the intercommunication and influence of each cell subset in the inflammatory process. Despite important advances in the understanding of the involvement of these cell types in MS, many questions still remain regarding the various subsets within each cell population and their exact contribution to different stages of the disease.

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Figures

Figure 1

Figure 1

Immune and glial cell subtypes and their contributions to the pathogenesis of EAE and MS. During the development and progression of EAE and MS, a variety of cells representing both the innate and adaptive immune system breach the blood brain barrier and invade the brain parenchyma. Resident glial cells also become activated and play an important role in the pathogenesis of EAE and MS. Some of the cell types involved are proinflammatory and promote demyelination, axonal damage, and the formation of disease plaques, whilst other cell types have anti-inflammatory and/or regulatory properties and inhibit disease progression by facilitating tissue repair.

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