CD8-mediated inflammatory central nervous system disorders

被引:13
作者
Willing, Anne [1 ]
Friese, Manuel A. [1 ]
机构
[1] Univ Klinikum Hamburg Eppendorf, Zentrum Mol Neurobiol, Inst Neuroimmunol & Klin MS Forsch, D-20251 Hamburg, Germany
关键词
autoimmunity; CD8; encephalitis; immunopathology; multiple sclerosis; T cell; CD8(+) T-CELLS; WEST-NILE-VIRUS; PLACEBO-CONTROLLED TRIAL; MULTIPLE-SCLEROSIS; JC VIRUS; RASMUSSEN ENCEPHALITIS; PREDICTS PROGNOSIS; CLASS-I; NATALIZUMAB; LEUKOENCEPHALOPATHY;
D O I
10.1097/WCO.0b013e328352ea8b
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review In central nervous system (CNS) autoimmune disorders, CD8(+) T cells have been reported to exert cytotoxic as well as regulatory functions. In virus-induced (meningo) encephalitis, they are essential for viral clearance, but can also cause severe immunopathology. This review aims to summarize the multifaceted roles CD8(+) T cells can play in inflammatory CNS disorders. Recent findings Recent evidence for a role of CD8(+) T cells in multiple sclerosis comes from genetic association studies confirming a protective effect of the HLA-A(+)0201 allele. Besides their dominance in white matter lesions, CD8(+) T cells contribute to immune infiltrates in cortical demyelinating lesions. Having infiltrated the CNS, CD8(+) T cells migrate along an inflammation-induced fibrous network. Although CD8(+) T cells are generally considered to be crucial for acute viral clearance, they can also induce autoimmune-like immunopathology by, for example, encountering a virus in adulthood while being at the same time latently infected by a related virus. Inadequate control of latent viruses under immunosuppressive treatments or immunodeficiencies is becoming increasingly important in neurology clinical work. Summary Future research should aim at identifying the specificity and functional phenotype of brain-infiltrating CD8(+) T cells in autoimmune diseases and viral immunopathology in order to develop therapeutic strategies specifically targeting CNS-relevant immune reactions.
引用
收藏
页码:316 / 321
页数:6
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