Eckner R J, Bennett M, Hettrick K L, Seidler C
J Virol. 1987 Aug;61(8):2631-8. doi: 10.1128/JVI.61.8.2631-2638.1987.
To determine whether hemopoietic cells infected with Friend polycythemia-inducing spleen focus-forming virus (SFFVp) are conserved or suppressed via natural surveillance in leukemia-resistant adult mice, we engrafted C57BL/6 recipients with isologous transgenic (donor origin marker) or natural killer (NK) cell-deficient B6 beige marrow cells exposed to SFFVp in vitro. Both groups of primary recipients were viremic and nonleukemic. Spleen cells from primary SFFVp-infected chimeras were engrafted into irradiated leukemia-susceptible secondary recipients to reveal dormant leukemia and grew as tumors of donor origin in 8 of 38 (21%) and 33 of 47 (70%) instances, respectively. Treatment of marrow donors and recipients with anti-asialo GM1 serum resulted in the depression of NK cell activity and the rapid development of dormant leukemia. We conclude that NK cells are an effective surveillance mechanism able to suppress SFFVp-induced preleukemic stem cells.
为了确定感染弗氏多血症诱导性脾集落形成病毒(SFFVp)的造血细胞在白血病抗性成年小鼠中是通过自然监测得以保存还是受到抑制,我们将体外暴露于SFFVp的同基因转基因(供体来源标记)或自然杀伤(NK)细胞缺陷的B6米色骨髓细胞移植到C57BL/6受体小鼠体内。两组初代受体小鼠均有病毒血症但无白血病。将初代感染SFFVp的嵌合体小鼠的脾细胞移植到经辐照的白血病易感二代受体小鼠体内,以揭示潜伏性白血病,结果分别有8/38(21%)和33/47(70%)的情况出现了供体来源的肿瘤生长。用抗去唾液酸GM1血清处理骨髓供体和受体,导致NK细胞活性降低以及潜伏性白血病的快速发展。我们得出结论,NK细胞是一种有效的监测机制,能够抑制SFFVp诱导的白血病前期干细胞。