Löhler J
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, F.R.G.
J Neuroimmunol. 1988 Dec;20(2-3):181-8. doi: 10.1016/0165-5728(88)90159-2.
Viral infections of the central nervous system (CNS), as of any other organ, evoke humoral and cellular immune responses which enable the host to eliminate the pathogen. However, effective responses may themselves produce tissue damage sometimes exceeding that caused by the virus itself. The relative contribution of the various immunopathological mechanisms in human viral encephalitides remains mostly ill defined. Most of our understanding of the immunopathogenesis in viral CNS infections comes from studies on experimentally infected animals. The prototype model of a virus-induced, cell-mediated, immunopathological CNS disease is the neurological illness of mice that follows intracerebral inoculation with lymphocytic choriomeningitis virus. Virus-specific cytotoxic T cells are crucial to the pathogenesis but death of the animals only results when these cells are targeted into functionally essential brain structures like the circumventricular organs or the medulla oblongata and cervical spinal cord.
与其他任何器官一样,中枢神经系统(CNS)的病毒感染会引发体液免疫和细胞免疫反应,使宿主能够清除病原体。然而,有效的免疫反应本身有时可能会造成组织损伤,这种损伤甚至超过病毒本身所造成的损害。在人类病毒性脑炎中,各种免疫病理机制的相对作用在很大程度上仍不明确。我们对病毒性中枢神经系统感染免疫发病机制的大多数了解来自对实验感染动物的研究。病毒诱导的、细胞介导的免疫病理中枢神经系统疾病的典型模型是小鼠在脑内接种淋巴细胞性脉络丛脑膜炎病毒后出现的神经系统疾病。病毒特异性细胞毒性T细胞对发病机制至关重要,但只有当这些细胞靶向进入功能重要的脑结构,如室周器官或延髓和颈脊髓时,动物才会死亡。