Sy M S, Tsurufuji M, Finberg R, Benacerraf B
J Immunol. 1983 Jul;131(1):30-6.
Infection of mice with vesicular stomatitis virus (VSV) at the time of immunization failed to enhance T cell-mediated immune response to azobenzenearsonate-(ABA) conjugated spleen cells as measured by delayed-type hypersensitivity and by in vitro proliferation and in vitro generation of ABA-specific cytotoxic T cells. However, mice infected with VSV are incapable of responding to signals from suppressor T cells or their soluble factors. Further analysis revealed that VSV infection does not interfere with the induction of Ts-1 or Ts-2 cells. Because infection of Ts-1 or Ts-2 donors had no effect on the subsequent response seen in the recipients of antigen and suppressor T cells, the most likely candidate for the target of VSV infection is therefore the Ts-3 cell or another T cell interacting with Ts-3. This is supported by our observation that it is possible to bypass the VSV effect by providing the recipients of VSV with normal Lyt-2+-bearing T cells.
在免疫时用水泡性口炎病毒（VSV）感染小鼠，未能增强T细胞介导的对偶氮苯胂酸盐-（ABA）偶联脾细胞的免疫反应，这是通过迟发型超敏反应、体外增殖以及ABA特异性细胞毒性T细胞的体外生成来衡量的。然而，感染VSV的小鼠无法对来自抑制性T细胞或其可溶性因子的信号作出反应。进一步分析表明，VSV感染不会干扰Ts-1或Ts-2细胞的诱导。由于感染Ts-1或Ts-2供体对随后在抗原和抑制性T细胞受体中观察到的反应没有影响，因此VSV感染的最可能靶点是Ts-3细胞或与Ts-3相互作用的另一种T细胞。我们的观察结果支持了这一点，即通过给感染VSV的受体提供正常的携带Lyt-2 +的T细胞，可以绕过VSV的作用。
