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Chapter 3 : Molecular Mimicry and Central Nervous System Autoimmune Disease
Infections have been associated with the initiation and/or exacerbation of multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS). It is suspected that tolerance to self-CNS antigens is broken by several linked events. This results in the initiation or induction of anti-CNS immune responses, which lead to inflammation and demyelination. Myelin basic protein (MBP) is a major component of CNS myelin, and when it is emulsified in adjuvant it can be used to induce experimental allergic encephalomyelitis (EAE) when it is injected into animals. Researchers found that 8 of 17 patients had lymphocytes that proliferated in response to MBP, whereas 6 of 40 individuals with measles without encephalomyelitis had such lymphocytes. Recently, other researchers extended the concept of molecular mimicry and autoimmune CNS disease. They have elegantly shown that the cross-reacting epitope between virus microbe and self-CNS protein does not need to have identical amino acids in order for T-cell recognition to occur. Theiler's murine encephalomyelitis virus (TMEV) infection of mice leads to a chronic demyelinating disease that has similarities to the human demyelinating disease MS. Early after infection natural killer (NK) cells can kill infected cells as part of the innate immune response. Viruses can cause direct lysis of infected cells through either apoptotic or necrotic pathways. Once an antiviral immune response develops, antiviral antibodies can bind to the surfaces of infected cells, leading to the activation of the complement cascade that eventually kills the infected cell.