Karupiah G, Blanden R V, Ramshaw I A
Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra, ACT.
J Exp Med. 1990 Nov 1;172(5):1495-503. doi: 10.1084/jem.172.5.1495.
Athymic nude mice recover from an infection with recombinant vaccinia virus (VV) encoding murine interleukin 2 (IL-2), but treatment with a mAb to IL-2 accentuated infection. Administration of a mAb against interferon gamma (IFN-gamma) to mice infected with the IL-2-encoding virus completely prevented the IL-2-induced mechanisms of recovery. Both asialo-GM1+ (NK) and asialo-GM1- (non-NK) cells were participants in the IFN-gamma-mediated recovery of nude mice from infection with the IL-2-encoding VV recombinant. Depletion of asialo-GM1+ cells exacerbated infection, though not as much as anti-IFN-gamma mAb. In vitro, both asialo-GM1+ and asialo-GM1- nude mouse splenocytes produced IFN-gamma in response to IL-2.
无胸腺裸鼠感染编码小鼠白细胞介素2(IL-2)的重组痘苗病毒(VV)后可恢复,但用抗IL-2单克隆抗体治疗会加重感染。给感染编码IL-2病毒的小鼠注射抗干扰素γ(IFN-γ)单克隆抗体可完全阻止IL-2诱导的恢复机制。脱唾液酸GM1 +(NK)细胞和脱唾液酸GM1 -(非NK)细胞都参与了IFN-γ介导的裸鼠从感染编码IL-2的VV重组体中恢复的过程。脱唾液酸GM1 +细胞的耗竭加剧了感染,尽管程度不如抗IFN-γ单克隆抗体。在体外,脱唾液酸GM1 +和脱唾液酸GM1 -裸鼠脾细胞对IL-2均产生IFN-γ。