Abstract
Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons. Historically, MS has been thought of as a T cell-mediated autoimmune disease of CNS white matter. However, recent studies have identified gray matter lesions in MS patients, suggesting that CNS antigens other than myelin proteins may be involved during the MS disease process. We have recently found that T cells targeting astrocyte-specific antigens can drive unique aspects of inflammatory CNS autoimmunity, including the targeting of gray matter and white matter of the brain and inducing heterogeneous clinical disease courses. In addition to being a target of T cells, astrocytes play a critical role in propagating the inflammatory response within the CNS induced NF-κB signaling. Here, we will discuss the pathophysiology of CNS inflammation mediated by T cell—glial cell interactions and its contributions to CNS autoimmunity.
Highlights
Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons
Susceptibility to MS is genetically linked to major histocompatibility complex (MHC) genes and genes associated with T cell activation and homeostasis; the strongest genetic linkage occurs with certain alleles of MHC class II, which suggests a direct relationship between autoreactive
The ability of myelin-reactive CD4 T cells to cause experimental autoimmune encephalomyelitis (EAE) further supports the hypothesis that myelin-reactive CD4 T cells have a central role in MS disease pathogenesis (Kuchroo et al, 2002; Sospedra and Martin, 2005; Ercolini and Miller, 2006; Hafler et al, 2007; Goverman, 2009; Steinman, 2009)
Summary
Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons. Further in support of this hypothesis, CD8 T cells specific for myelin proteins, including MBP, MOG, and PLP, have been shown to be pathogenic in several animal models of CNS disease (Huseby et al, 2001a; Sun et al, 2001; Ford and Evavold, 2005; Friese et al, 2008; Anderson et al, 2012).
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