Key result
Class I-deficient mice had significantly more disease in white matter areas compared to Class II-deficient mice, while antibody protected the striatum from TMEV-induced pathology.
Distinct immune system components function to protect discrete areas of the central nervous system from virus-induced pathology.
Highlights compartmentalized CNS immune protection in viral models; hypothesis-generating for human neuroinflammatory therapies.
The basis for the distinct patterns of brain pathology in individuals experiencing virus-induced encephalitis may be related to either the tropism of the virus or the host's response to virus infection of the central nervous system (CNS). In these studies we used Theiler's murine encephalomyelitis virus (TMEV) and a series of mice deficient in various immune system components (alpha/beta T cells, antibody, Class I MHC, and Class II MHC) to examine the hypothesis that discrete populations of CNS cells are protected differentially from virus infection by distinct arms of the immune response. Here we demonstrate that the Class I-mediated immune response provided more protection from areas of the brain (brainstem, corpus callosum and cerebellum) with abundant white matter as there was significantly more disease in these areas in beta2m -/- (Class I-deficient) mice as compared to A beta(0) (Class II-deficient) mice. In contrast, the striatum, with an abundance of neurons, was protected from virus-induced pathology primarily by antibody. In addition, we determined that antibody and alpha/beta T cells provided protection from severe deficits and death during the acute phase of the disease. The data presented here support the hypothesis that distinct immune system components function to protect discrete areas of the CNS from virus-induced pathology.
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Drescher et al. (1999) studied Virus-induced encephalitis. Immune system component deficiencies vs. Other immune deficiencies (e.g., Class I-deficient vs Class II-deficient) was evaluated on Virus-induced pathology in discrete CNS areas. Class I-deficient mice had significantly more disease in white matter areas compared to Class II-deficient mice, while antibody protected the striatum from TMEV-induced pathology.
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