Fujisawa H, Kumazawa Y, Ohtani A, Nishimura C
J Clin Lab Immunol. 1984 Jan;13(1):41-6.
The relationship between the development of virus plaque forming cells (V-PFC) and the blastogenic response of T cells activated with concanavalin A (Con A) was investigated in connection with the cell cycle using a modified virus plaque assay (VPA) which facilitated the quantitative detection of T lymphoblasts with low susceptibility to infection by vesicular stomatitis virus (vsv). The generation of V-PFC markedly decreased when DNA synthesis inhibitors such as thymidine, hydroxyurea and cytosine arabinoside (Ara C) were added to spleen cell cultures stimulated with Con A, while the addition of a mitotic inhibitor, Colcemid, to the cultures caused only partial reduction of V-PFC development. These results indicate that the S to G2 phases of the first cell cycle are essential for vsv-replication or V-PFC development in Con A activated T cells. However, vsv-replication in the activated T cells does not depend on the initial G1 phase during the blastogenic response since the morphological blast formation of activated T cells is not suppressed by treatment with DNA synthesis inhibitors.
使用改良的病毒蚀斑测定法(VPA),结合细胞周期,研究了病毒蚀斑形成细胞(V-PFC)的发育与用伴刀豆球蛋白A(Con A)激活的T细胞的增殖反应之间的关系,该方法有助于定量检测对水疱性口炎病毒(VSV)感染敏感性较低的T淋巴母细胞。当将诸如胸苷、羟基脲和阿糖胞苷(Ara C)等DNA合成抑制剂添加到用Con A刺激的脾细胞培养物中时,V-PFC的生成显著减少,而向培养物中添加有丝分裂抑制剂秋水仙酰胺仅导致V-PFC发育部分减少。这些结果表明,在Con A激活的T细胞中,第一个细胞周期的S期到G2期对于VSV复制或V-PFC发育至关重要。然而,激活的T细胞中的VSV复制并不依赖于增殖反应期间最初的G1期,因为DNA合成抑制剂处理不会抑制激活的T细胞的形态学母细胞形成。