Effect of vesicular stomatitis virus (VSV) infection on the development and regulation of T cell-mediated immune responses.
Effect of vesicular stomatitis virus (VSV) infection on the development and regulation of T cell-mediated immune responses.
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DOI：
10.4049/jimmunol.131.1.30
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发表时间：
1983-07
影响因子：
4.4
通讯作者：
M. Sy;M. Tsurufuji;R. Finberg;B. Benacerraf
中科院分区：
文献类型：
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作者：
M. Sy;M. Tsurufuji;R. Finberg;B. Benacerraf
水泡性口炎病毒(VSV)免疫小鼠后，通过迟发型超敏反应、ABA特异性细胞毒性T细胞的体外增殖和体外产生，均未能增强偶氮苯基亚胺(ABA)结合的脾细胞的T细胞免疫应答。然而，感染VSV的小鼠不能对抑制性T细胞或其可溶性因子的信号做出反应。进一步分析表明，VSV感染不干扰ts-1或ts-2细胞的诱导。由于ts-1或ts-2供者的感染对抗原和抑制T细胞受体的后续反应没有影响，因此最有可能成为VSV感染目标的是ts-3细胞或与ts-3相互作用的另一个T细胞。我们的观察结果支持了这一点，即可以通过为VSV的接受者提供正常的Lyt-2+T细胞来绕过VSV效应。
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.