Cellular interactions in the cytotoxic T lymphocyte response to herpes simplex virus antigens: differential antigen activation requirements for the helper T lymphocyte and cytotoxic T lymphocyte precursors.
Cellular interactions in the cytotoxic T lymphocyte response to herpes simplex virus antigens: differential antigen activation requirements for the helper T lymphocyte and cytotoxic T lymphocyte precursors.
复制标题
细胞毒性 T 淋巴细胞对单纯疱疹病毒抗原反应中的细胞相互作用：辅助 T 淋巴细胞和细胞毒性 T 淋巴细胞前体的不同抗原激活要求。
作者：
D. Schmid;B. Rouse
研究了辅助性T淋巴细胞对单纯疱疹病毒1型(HSV-1)免疫应答的作用和诱导条件。来自体内感染HSV-1的小鼠的脾细胞可以在体外与活的或部分紫外线灭活的HSV-1重新刺激，以产生高水平的疱疹病毒特异性细胞毒性T淋巴细胞(CTL)活性。相比之下，单纯的脾细胞或来自热灭活HSV-1的小鼠脾细胞在体外病毒刺激后不能产生CTL。此外，用抗Lyt-1抗血清加补体预处理，可使感染HSV免疫的脾细胞对二次体外再刺激无反应。脾细胞取自体内感染了传染性HSV-1的小鼠，这些小鼠已经被启动并重新刺激。第二次预充后两天，取脾细胞进行照射。在上述所有无反应的细胞群中，这些细胞都能够不同程度地协助CTL的产生。当单独与抗原一起培养时，受照射的细胞不产生可检测到的CTL活性。此外，如果照射的脾细胞在加入培养物之前用抗Lyt-1加补体处理，所有恢复活性都被消融。相比之下，在体内用热灭活或紫外线灭活的HSV-1启动和重新刺激的小鼠的照射后的脾细胞，无法为幼稚或辅助耗尽的培养提供帮助。未能提供辅助活性似乎并不涉及抑制细胞的优先激活，这一点从细胞混合实验和将浓缩的、抗原刺激的脾细胞上清液添加到次级抗HSV-1脾细胞培养中得到了证明。用白介素2(IL-2)依赖的细胞系作为相对辅助活性的增殖分析表明，灭活形式的HSV-1不能有效地征集辅助活性。因此，这些实验表明，观察到的热灭活或紫外线灭活的HSV-1制剂未能诱导抗HSV CTL反应，反映了HSV-1特异性辅助T淋巴细胞亚群无法识别这些形式的抗原。
The role and induction requirements of helper T lymphocyte responses to herpes simplex virus type 1 (HSV-1) was examined. Splenocytes from mice that had been primed in vivo with infectious HSV-1 can be restimulated in vitro with live or partially UV-inactivated HSV-1 to generate high levels of herpes virus-specific cytotoxic T lymphocyte (CTL) activity. By comparison, naive splenocytes or splenocytes taken from mice primed with heat-inactivated HSV-1 failed to generate CTL after in vitro viral stimulation. In addition, infectious HSV-primed splenocytes can be rendered unresponsive to secondary in vitro restimulation by pretreatment with anti-Lyt-1 antiserum plus complement. Spleen cells were taken from mice that had been primed and restimulated in vivo with infectious HSV-1. Two days after the second priming, splenocytes were prepared and irradiated. These cells were capable of assisting in the generation of CTL to varying degrees in all of the above unresponsive populations of cells. The irradiated cells did not produce detectable levels of CTL activity when cultured alone with antigen. Also, if the irradiated splenocytes were treated with anti-Lyt-1 plus complement before their addition to cultures, all restorative activity was ablated. In contrast, irradiated splenocytes from mice that had been primed and restimulated in vivo with either heat-inactivated or UV-inactivated HSV-1 were unable to provide help to naive or helper-depleted cultures. The failure to supply helper activity appears not to involve the preferential activation of suppressor cells, as evidenced by cell mixing experiments and the addition of concentrated, antigen-stimulated spleen cell supernatant fluids to secondary anti-HSV-1 splenocyte cultures. Proliferative assays using interleukin 2- (IL 2) dependent cell lines as a measure of relative helper activity indicated that the inactivated forms of HSV-1 were incapable of effectively enlisting helper activity. These experiments therefore suggest that the observed failure of heat-inactivated or UV-inactivated HSV-1 preparations to induce anti-HSV CTL responses reflects the inability of the HSV-1-specific subset of helper T lymphocytes to recognize these forms of the antigen.