Ofir R, Weinstein Y, Rager-Zisman B
Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel.
Nat Immun Cell Growth Regul. 1988;7(2):77-86.
The role of natural killer (NK) cells in retrovirus-induced leukemogenesis was studied. These cells which do not require prior sensitization are considered as a part of the body's defense system against tumor development and spread. Neonate BALB/c mice infected with Moloney murine leukemia virus (MoLV) develop leukemia within 3-6 months. The MoLV-infected mice showed a progressive loss of endogenous and augmented NK activity, correlated with the development of the leukemic state. Mixing of spleen cells from tumor-bearing mice with NK-augmented splenocytes resulted in suppression of NK activity. In addition, mixing of T cell lines isolated from MoLV-induced tumors with augmented splenocytes also resulted in the down-regulation of NK cell activity. The present study demonstrates that tumor cells from leukemic organs and leukemic T cell lines can actively suppress NK cell function. It is postulated that after MoLV infection the progression of virus-transformed T cells to a fully developed tumor depends on the ability of these cells to down-regulate NK cell activity and thus escape immune surveillance.
研究了自然杀伤(NK)细胞在逆转录病毒诱导白血病发生中的作用。这些无需预先致敏的细胞被视为机体抗肿瘤发生和扩散防御系统的一部分。感染莫洛尼鼠白血病病毒(MoLV)的新生BALB/c小鼠在3 - 6个月内会发生白血病。感染MoLV的小鼠内源性NK活性逐渐丧失且活性增强,这与白血病状态的发展相关。将荷瘤小鼠的脾细胞与NK活性增强的脾细胞混合会导致NK活性受到抑制。此外,将从MoLV诱导的肿瘤中分离出的T细胞系与活性增强的脾细胞混合也会导致NK细胞活性下调。本研究表明,白血病器官的肿瘤细胞和白血病T细胞系可主动抑制NK细胞功能。据推测,MoLV感染后,病毒转化的T细胞发展为完全成熟肿瘤的进程取决于这些细胞下调NK细胞活性从而逃避免疫监视的能力。