Tripp R A, Sarawar S R, Doherty P C
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
J Immunol. 1995 Sep 15;155(6):2955-9.
The development of influenza virus-specific CD8+ cytotoxic T lymphocyte precursors (CTLp) is diminished in H-2b mice that are homozygous (-/-) for disruption of the H-2lAb gene. Virus clearance was not obviously delayed when compared with the congenic H-2lAb (+/+) controls, and evidence of CTL activity was apparent for inflammatory cells recovered from the respiratory tract in both cases. However, the virus-specific CTLp that are normally present in the regional lymph nodes and in the infected lung were evidently being consumed at the peak of the host response to give the terminally differentiated CTL effectors. Even so, any exhaustion of the CTLp pool was apparently transitory with this localized infection as, though the frequencies were consistently lower than those found for the (+/+) controls, CTLp could be detected reproducibly in both lymph nodes and spleen through 14 mo after infection. Analysis of cytokine profiles during the acute response showed a substantial defect in the (-/-) mice, indicating that cytokine production is largely dependent on the influenza-specific CD4+ set.
在H-2lAb基因破坏纯合（-/-）的H-2b小鼠中，流感病毒特异性CD8 +细胞毒性T淋巴细胞前体（CTLp）的发育减少。与同基因H-2lAb（+/+）对照相比，病毒清除没有明显延迟，并且在两种情况下从呼吸道回收的炎性细胞都有明显的CTL活性证据。然而，通常存在于区域淋巴结和感染肺中的病毒特异性CTLp在宿主反应的高峰期显然被消耗，以产生终末分化的CTL效应细胞。即便如此，对于这种局部感染，CTLp库的任何耗竭显然都是暂时的，因为尽管其频率始终低于（+/+）对照，但在感染后14个月内，在淋巴结和脾脏中均可重复检测到CTLp。急性反应期间细胞因子谱分析显示（-/-）小鼠存在实质性缺陷，表明细胞因子产生在很大程度上依赖于流感特异性CD4 +细胞群。
