Koszinowski U, Greber D, Neuschaefer-Rube I
Immunobiology. 1979 Aug;156(1-2):83-95.
Cytotoxic T lymphocytes (CTL) from DBA/2 strain mice primed with Sendai virus (SV) in vivo were activated by secondary stimulation of spleen cells with viral antigens in vitro and analyzed for their target antigen specificity. These effector cells lysed syngeneic Sendai virus infected target cells, marginally a variety of non-infected targets and had a strong cytotoxic effect on H-2b targets. Studies on the antigenic requirements revealed that all SV preparations which generated specific CTL also induced the alloreactive populations. Similar results were found in the response to Newcastle disease virus (NDV) and some influenza A viruses; all these viruses were mitogenic for lymphocytes. Experiments on the cellular requirements indicated that virus specific and alloreactive cells can be separated by their requirements for help and for restimulation. By competition experiments both activities could be attributed to clearly separable T cell subpopulations. The induction mechanism of alloreactive T cells by viral antigens is discussed.
用仙台病毒（SV）在体内致敏的DBA/2品系小鼠的细胞毒性T淋巴细胞（CTL），通过体外病毒抗原对脾细胞的二次刺激而被激活，并对其靶抗原特异性进行分析。这些效应细胞裂解同基因的仙台病毒感染的靶细胞，对多种未感染的靶细胞有轻微作用，对H-2b靶细胞有强烈的细胞毒性作用。对抗原需求的研究表明，所有产生特异性CTL的SV制剂也诱导了同种异体反应性群体。在对新城疫病毒（NDV）和一些甲型流感病毒的反应中也发现了类似结果；所有这些病毒对淋巴细胞都有促有丝分裂作用。对细胞需求的实验表明，病毒特异性细胞和同种异体反应性细胞可以根据它们对辅助和再刺激的需求进行分离。通过竞争实验，这两种活性都可归因于明显可分离的T细胞亚群。本文讨论了病毒抗原诱导同种异体反应性T细胞的机制。
