Heterosubtypic immunity to influenza type A virus in mice. Effector mechanisms and their longevity.
Heterosubtypic immunity to influenza type A virus in mice. Effector mechanisms and their longevity.
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DOI：
10.4049/jimmunol.152.4.1653
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发表时间：
1994-02
影响因子：
4.4
通讯作者：
S. Liang;K. Mozdzanowska;G. Palladino;W. Gerhard
中科院分区：
文献类型：
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作者：
S. Liang;K. Mozdzanowska;G. Palladino;W. Gerhard
在不同亚型的甲型流感病毒之间发生交叉反应的免疫称为异(亚)型(Het-I)。我们通过用异亚型病毒X31攻击PR8免疫小鼠来研究Het-I。HET-I不能预防X31感染，但在感染高峰期，它对康复有很大的帮助。通过同时攻击X31和一种免疫无关的B型流感病毒，以及在攻击前耗尽PR8免疫小鼠的单个淋巴细胞亚群，研究了所涉及的效应机制的性质。研究表明：1)效应机制与免疫识别事件密切相关。2)在鼻腔中，CD8+或CD4+T细胞的耗尽导致Het-I的部分减少，同时两个T细胞亚群的同时耗尽几乎完全消除了Het-I。这种T细胞介导的免疫是短暂的，在诱导后4-5个月消失。3)在气管和肺中，CD8+T细胞的耗竭导致Het-I的部分下降，而CD4+T细胞的耗竭对Het-I的影响不明显。CD8介导的成分似乎是短暂的，而残余免疫(在CD4/8耗尽的小鼠中)是长期存在的，并在诱导后持续7个月以上。4)去除NK细胞不会显著降低鼻和肺组织中Het-I的表达强度。总之，这项研究表明，Het-I在这个系统中是由一种复杂的免疫机制组合介导的，这些机制在一定程度上不同于上呼吸道和下呼吸道。
Immunity that cross-reacts between influenza type A viruses of distinct subtypes is called hetero(sub)typic (Het-I). We have studied Het-I by challenging PR8-immune mice with the heterosubtypic virus X31. Het-I did not prevent infection by X31 but, at its height, strongly aided in recovery. The nature of the effector mechanisms involved was investigated by simultaneous challenge with X31 and an immunologically unrelated influenza type B virus and by depleting individual lymphocyte subsets in PR8-immune mice before challenge. The study showed the following: 1) The effector mechanisms were intimately associated with immune recognition events. 2) In the nose, depletion of CD8+ or CD4+ T cells led to partial reduction of Het-I, and simultaneous depletion of both T cell subsets abrogated Het-I almost completely. This T cell-mediated immunity was short lived and had disappeared 4 to 5 mo after induction. 3) In trachea and lung, depletion of CD8+ T cells led to a partial reduction of Het-I, whereas depletion of CD4+ T cells was without significant effect. The CD8-mediated component appeared short lived, whereas the residual immunity (in CD4/8-depleted mice) was long lived and persisted past 7 mos after induction. 4) Depletion of NK cells did not significantly reduce the strength of Het-I in either nose or lung. In conclusion, the study shows that Het-I in this system is mediated by a complex combination of immune mechanisms that differ, in part, between upper and lower respiratory tract.