Thomas I K, Erickson K L
J Natl Cancer Inst. 1985 Mar;74(3):675-80.
For understanding the mechanism by which fatty acids promote mammary tumor growth, experiments were designed to determine the influence of dietary fat concentration and saturation on both effector (Ef) and target (Ta) cells in an allogeneic antitumor cell-mediated immune response. Exposure of cytotoxic T-lymphocytes (CTL) to different fatty acids led to significant changes in the subsequent cytolytic capacity of these cells after both primary and secondary immunization. An increase in both saturated (SF) and polyunsaturated (PUF) fats led to decreased cytotoxic function after primary immunization. After a secondary challenge, the suppressive influence of SF was significantly greater than that of PUF, compared to that of the control diet containing essential fatty acids as the only fat source. This response was mediated by a direct effect on the CTL and not through an increase in suppressor or a decrease in Ef or helper cell frequency. In contrast, manipulation of the fatty acid environment of the Ta mammary tumor cells in vivo or in vitro had no significant effect on their susceptibility to lymphocyte-mediated cytotoxicity. Therefore, dietary fats may mediate their effect by a direct influence on the immunocompetent lymphocyte and not on the Ta mammary tumor cell.
为了解脂肪酸促进乳腺肿瘤生长的机制，设计了实验来确定饮食中脂肪浓度和饱和度对同种异体抗肿瘤细胞介导的免疫反应中效应细胞（Ef）和靶细胞（Ta）的影响。细胞毒性T淋巴细胞（CTL）暴露于不同脂肪酸后，在初次和二次免疫后这些细胞随后的细胞溶解能力发生了显著变化。饱和脂肪（SF）和多不饱和脂肪（PUF）的增加均导致初次免疫后细胞毒性功能降低。二次攻击后，与以必需脂肪酸作为唯一脂肪来源的对照饮食相比，SF的抑制作用明显大于PUF。这种反应是由对CTL的直接作用介导的，而不是通过增加抑制细胞或降低Ef或辅助细胞频率来实现的。相反，体内或体外对Ta乳腺肿瘤细胞的脂肪酸环境进行调控，对其对淋巴细胞介导的细胞毒性的敏感性没有显著影响。因此，饮食脂肪可能通过直接影响免疫活性淋巴细胞而非Ta乳腺肿瘤细胞来介导其作用。
