Measles virus-induced suppression of immune responses.
Measles virus-induced suppression of immune responses.
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DOI：
10.1111/j.1600-065x.2010.00925.x
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发表时间：
2010-07
影响因子：
8.7
通讯作者：
Griffin DE
中科院分区：
文献类型：
--
作者：
Griffin DE
麻疹是儿童死亡的一个重要原因，它与免疫系统有着看似矛盾的相互作用。在大多数个体中，免疫反应最终成功清除麻疹病毒（MV）感染并建立终生免疫力。然而，感染还与病毒RNA的持续存在和数周的免疫抑制有关，包括迟发型超敏反应的丧失和继发感染的易感性增加。最初的 T 细胞反应包括 CD8+ 和辅助 T 1 CD4+ T 细胞，对于控制传染性病毒很重要。随着病毒 RNA 的持续存在，T 辅助细胞 2 CD4+ T 细胞反应会发生转变，这可能会促进 B 细胞成熟和持久的抗体反应，但可能会抑制巨噬细胞激活和 T 辅助细胞 1 对新感染的反应。对有丝分裂原诱导的淋巴细胞增殖的抑制可以通过用MV感染淋巴细胞或通过在没有感染的情况下将淋巴细胞暴露于血凝素和融合表面糖蛋白的复合物来诱导。树突状细胞容易受到感染，并且可以将感染传播至淋巴细胞。 MV 感染的树突状细胞无法刺激混合淋巴细胞反应，并且可以通过 MV 糖蛋白的表达诱导淋巴细胞无反应。因此，多种因素可能会导致麻疹引起的免疫抑制和持久保护性免疫力的建立。
Measles is an important cause of child mortality that has a seemingly paradoxical interaction with the immune system. In most individuals, the immune response is successful in eventually clearing measles virus (MV) infection and in establishing life-long immunity. However, infection is also associated with persistence of viral RNA and several weeks of immune suppression, including loss of delayed type hypersensitivity responses and increased susceptibility to secondary infections. The initial T-cell response includes CD8+ and T-helper 1 CD4+ T cells important for control of infectious virus. As viral RNA persists, there is a shift to a T-helper 2 CD4+ T-cell response that likely promotes B-cell maturation and durable antibody responses but may suppress macrophage activation and T-helper 1 responses to new infections. Suppression of mitogen-induced lymphocyte proliferation can be induced by lymphocyte infection with MV or by lymphocyte exposure to a complex of the hemagglutinin and fusion surface glycoproteins without infection. Dendritic cells are susceptible to infection and can transmit infection to lymphocytes. MV-infected dendritic cells are unable to stimulate a mixed lymphocyte reaction and can induce lymphocyte unresponsiveness through expression of MV glycoproteins. Thus, multiple factors may contribute both to measles-induced immune suppression and to the establishment of durable protective immunity.