Askonas B A, Mullbacher A, Ashman R B
Immunology. 1982 Jan;45(1):79-84.
Infective influenza virus primes mice and increases at least ten-fold the level of splenic cytotoxic T-memory and precursor cells in comparison with normal mice. Intranasal virus infection or intraperitoneal injection of infective virus results in frequencies of 1-2 x 10(-4) cytotoxic T-cell precursors in spleen as determined by limiting dilution assays. With both types of immunization, T-helper cells amplifying the generation of T-killer cells are limiting, and optimal clone frequencies depend on addition of excess T-helper cells. We find that at least part of the T-helper cells amplifying the generation of cytotoxic T cells are cross reactive for the type A influenza viruses and therefore have a similar virus specificity to type A influenza-specific cytotoxic T cells (tc). Help for T-killer cells can be replaced by supernatants derived from Concanavalin A-stimulated rat spleen cells, but presence of antigen is still required to stimulate the Tc precursor or memory cells before they respond to antigen non-specific T cell-growth factor(s) present in the stimulated rat spleen cell medium.
感染性流感病毒可使小鼠致敏,并使其脾脏细胞毒性T记忆细胞和前体细胞水平比正常小鼠至少增加十倍。通过有限稀释分析测定,经鼻内病毒感染或腹腔注射感染性病毒后,脾脏中细胞毒性T细胞前体的频率为1-2×10⁻⁴。两种免疫方式中,扩增T杀伤细胞生成的T辅助细胞均有限,最佳克隆频率取决于添加过量的T辅助细胞。我们发现,至少部分扩增细胞毒性T细胞生成的T辅助细胞对甲型流感病毒具有交叉反应性,因此与甲型流感特异性细胞毒性T细胞(Tc)具有相似的病毒特异性。对T杀伤细胞的辅助作用可被伴刀豆球蛋白A刺激的大鼠脾细胞衍生的上清液替代,但在Tc前体细胞或记忆细胞对刺激的大鼠脾细胞培养基中存在的抗原非特异性T细胞生长因子作出反应之前,仍需要抗原的存在来刺激它们。