Dunlop M B, Blanden R V
Immunology. 1976 Aug;31(2):171-80.
Secondary (memory) cell-mediated cytotoxic responses in lymphoid cells from CBA/H mice pre-primed with lymphocytic choriomeningitis virus (LCM) 5-7 weeks previously were induced by culturing these cells in vitro with syngeneic, infected peritoneal cells at 37 degrees for periods of up to 5 days. Cytotoxic effectors were assayed against LCM infected, H-2 compatible target cells in a 51Cr release assay. Response was greater with a higher ratio (1:10) of infected peritoneal cells:pre-primed cells than with lower ratios (e.g. 1:250). Separating responders from infected cells by a 450 mmum nucleopore membrane (coarse enough to allow passage of virus particles) still permitted induction of a secondary response whilst interposition of a 50 mmum nucleopore membrane (which apparently prevented transit of virus particles) virtually abolished the secondary response. Removal of phagocytic cells from responders prior to setting up memory cultures greatly reduced responders' capacity to be induced. Fixed, infected stimulators still induced strong secondary responses. Secondary response was maximal with spleen cells, peripheral blood lymphocytes, or pooled iliac and lumbar lymph node cells. Thymocytes responded less well, whilst mesenteric lymphoid cells and peritoneal cells gave minimal responses. Effector cells from memory cultures killed targets with single-hit kinetics and a rectilinear log effectors: log targets lysed relation held. Memory spleen cells developed increasing cytolytic activity from 2 to 5 days in culture. Memory-generated effectors were markedly potent by day 5, e.g. giving 70 per cent specific release at a killer:target ratio of 0-8:1. Peak DNA synthesis occurred on day 4. We conclude that memory effectors as a population differ in kinetics and potency from effectors obtained by primary viral challenge in the mouse.
5至7周前用淋巴细胞性脉络丛脑膜炎病毒(LCM)预先致敏的CBA/H小鼠的淋巴细胞中的继发性(记忆性)细胞介导的细胞毒性反应,是通过将这些细胞与同基因的、感染的腹腔细胞在37℃体外培养长达5天来诱导的。在51Cr释放试验中,针对LCM感染的、H-2相容的靶细胞检测细胞毒性效应细胞。感染的腹腔细胞与预先致敏细胞的比例为1:10时的反应比比例较低(如1:250)时更强。用450μm核孔膜(粗到足以允许病毒颗粒通过)将反应细胞与感染细胞分开,仍可诱导继发性反应,而插入50μm核孔膜(显然可阻止病毒颗粒通过)实际上消除了继发性反应。在建立记忆培养之前从反应细胞中去除吞噬细胞,会大大降低反应细胞被诱导的能力。固定的、感染的刺激细胞仍能诱导强烈的继发性反应。脾脏细胞、外周血淋巴细胞或汇集的髂骨和腰淋巴结细胞的继发性反应最大。胸腺细胞反应较差,而肠系膜淋巴细胞和腹腔细胞的反应最小。记忆培养产生的效应细胞以单次打击动力学杀死靶细胞,并且效应细胞对数与裂解靶细胞对数之间呈直线关系。记忆性脾脏细胞在培养2至5天期间产生的溶细胞活性不断增加。到第5天,记忆产生的效应细胞明显具有效力,例如在杀伤细胞与靶细胞比例为0.8:1时可产生70%的特异性释放。DNA合成高峰出现在第4天。我们得出结论,作为一个群体的记忆效应细胞在动力学和效力方面与通过小鼠原发性病毒攻击获得的效应细胞不同。