CELL MEDIATED IMMUNITY IN INFLUENZA

汉坦病毒和耐药病毒的最新经验 肺结核突出表明我们易受呼吸道病原体的侵害。 我们忘记了本世纪最大的病毒大流行是由任何 A型流感病毒，这些病毒杀死大量的 人每年。 豁免权是我们唯一的保护： 行为矫正可以防止高传染性的 城市人群中的呼吸道病毒。 尽管如此，少数 现有的疫苗是次优的，反映了我们基本缺乏 了解如何最好地促进有效的免疫反应， 呼吸道粘膜 这一建议继续系统地、定量地 小鼠肺和淋巴组织中细胞事件的解剖 感染了甲型流感病毒。 大量新颖的信息 在上一个融资周期中出现。 这种严格的体内开发 模型被证明在显示微妙但重要的影响方面具有巨大价值 在（例如）基因被破坏的“敲除”小鼠中。 正在进行的 实验集中在响应的进一步定义上 病毒特异性CD4+和 CD8+ α β T细胞受体（TCR）+淋巴细胞，这些T细胞的命运 细胞和各种细胞因子的作用。 分析将不可避免地 提供了对细胞介导的免疫性质的进一步了解， 一般情况下，病毒清除的特点与病理学有关 与这种免疫反应，并提出免疫可能是 通过操纵正常的宿主抗性机制来增强。

Recent experience with the hantaviruses and with drug-resistant tuberculosis has emphasized our vulnerability to respiratory pathogens. We forget that the greatest virus pandemic in this century was caused any an influenza A virus, and that these viruses kill substantial numbers of people each year. Immunity is our only protection: no amount of behavioral modification can prevent the spread of a highly infectious respiratory virus within urban populations. Despite this, the few vaccines that are available are sub-optimal, reflecting our basic lack of understanding of how best to promote an effective immune response at the respiratory mucosa. This proposal continues the systematic, quantitative dissection of the cellular events in the lung and lymphoid tissue of mice infected with influenza A viruses. Substantial, novel information has emerged in the previous funding period. This rigorously developed in vivo model is proving of great value for showing subtle, but important, effects in (for instance) genetically disrupted "knock-out" mice. The on-going experiments concentrate on the further definition of the response characteristics and effector mechanisms used by virus-specific CD4+ and CD8+ alpha beta T cell receptor (TCR)+ lymphocytes, the fate of these T cells and the roles of various cytokines. The analysis will inevitably provide further insights into the nature of cell-mediated immunity in general, the characteristics of virus clearance and pathology associated with this immune response, and suggest ways that immunity might be enhanced by manipulating normal host resistance mechanisms.