Aichele Peter, Unsoeld Heike, Koschella Marie, Schweier Oliver, Kalinke Ulrich, Vucikuja Smiljka
Institute for Medical Microbiology and Hygiene, Department of Immunology, University of Freiburg, Freiburg, Germany.
J Immunol. 2006 Apr 15;176(8):4525-9. doi: 10.4049/jimmunol.176.8.4525.
The role of type I IFN signaling in CD8 T cells was analyzed in an adoptive transfer model using P14 TCR transgenic CD8 T cells specific for lymphocytic choriomeningitis virus (LCMV) but deficient in type I IFNR. In the present study, we demonstrate severe impairment in the capacity of P14 T cells lacking type I IFNR to expand in normal type I IFNR wild-type C57BL/6 hosts after LCMV infection. In contrast, following infection of recipient mice with recombinant vaccinia virus expressing LCMV glycoprotein, P14 T cell expansion was considerably less dependent on type I IFNR expression. Lack of type I IFNR expression by P14 T cells did not affect cell division after LCMV infection but interfered with clonal expansion. Thus, direct type I IFN signaling is essential for CD8 T cell survival in certain viral infections.
在一个过继转移模型中,利用对淋巴细胞性脉络丛脑膜炎病毒(LCMV)特异但缺乏I型干扰素受体(IFNR)的P14 TCR转基因CD8 T细胞,分析了I型干扰素信号在CD8 T细胞中的作用。在本研究中,我们证明,缺乏I型IFNR的P14 T细胞在LCMV感染后,在正常I型IFNR野生型C57BL/6宿主中扩增的能力严重受损。相反,在用表达LCMV糖蛋白的重组痘苗病毒感染受体小鼠后,P14 T细胞的扩增对I型IFNR表达的依赖性大大降低。P14 T细胞缺乏I型IFNR表达并不影响LCMV感染后的细胞分裂,但会干扰克隆扩增。因此,直接的I型干扰素信号对于某些病毒感染中CD8 T细胞的存活至关重要。