Droller M J, Gomolka D
Cell Immunol. 1984 Jun;86(1):242-50. doi: 10.1016/0008-8749(84)90376-9.
The effect of polyinosinic . polycytidylic acid [poly(I:C)] on tumor inhibition in the context of natural cytotoxicity enhancement prompted further assessment of mechanisms underlying these effects. In vivo inoculations of poly(I:C) led to dose-dependent cytotoxicity enhancement in splenic lymphocytes and nonrecruited peritoneal exudate cells (monocytes). Although cytotoxicity of macrophages and lymphocytes together was less than that seen with lymphocytes alone, addition of indomethacin to these samples did not enhance cytotoxicity. In vivo inoculation of anti-interferon prior to poly(I:C) treatment prevented poly(I:C)-induced enhancement of natural cytotoxicity. Tumor growth was significantly inhibited by poly(I:C) treatment. Prior inoculation of anti-interferon antiserum partially prevented such tumor inhibition. Taken together, the tumor-inhibitory effect of poly(I:C) in this model may be mediated by interferon production and, at least in part, by interferon-induced enhancement of natural cytotoxicity.
聚肌苷酸.聚胞苷酸[聚（I：C）]在增强自然细胞毒性的情况下对肿瘤抑制的作用促使人们进一步评估这些作用背后的机制。体内接种聚（I：C）导致脾淋巴细胞和未募集的腹腔渗出细胞（单核细胞）中细胞毒性呈剂量依赖性增强。尽管巨噬细胞和淋巴细胞共同的细胞毒性小于单独淋巴细胞的细胞毒性，但向这些样本中添加消炎痛并未增强细胞毒性。在聚（I：C）处理之前体内接种抗干扰素可阻止聚（I：C）诱导的自然细胞毒性增强。聚（I：C）处理可显著抑制肿瘤生长。预先接种抗干扰素抗血清可部分阻止这种肿瘤抑制。综上所述，聚（I：C）在该模型中的肿瘤抑制作用可能由干扰素产生介导，并且至少部分由干扰素诱导的自然细胞毒性增强介导。
