Yamamoto T, Yamamoto S, Kataoka T, Tokunaga T
Department of Bacterial and Blood Products, National Institute of Health, Tokyo, Japan.
Microbiol Immunol. 1994;38(10):831-6. doi: 10.1111/j.1348-0421.1994.tb01867.x.
A synthetic 22-mer oligodeoxyribonucleotide having an AACGTT palindrome, AAC-22, induced interferon (IFN) production and augmented the natural killer (NK) activity in murine splenocytes, whereas its analogue, ACC-22, having an ACCGGT palindrome, did not. The binding of AAC-22 to splenocytes was not different from that of ACC-22. Lipofection of AAC-22 to splenocytes remarkably enhanced IFN production and NK cell activity, whereas that of ACC-22 caused little enhancement. These results strongly suggest that the prerequisite for IFN production is not the binding of AAC-22 to the cell surface receptors, but its penetration into the spleen cells.
一种具有AACGTT回文序列的合成22聚体寡脱氧核糖核苷酸AAC-22，可诱导小鼠脾细胞产生干扰素（IFN）并增强自然杀伤（NK）活性，而其具有ACCGGT回文序列的类似物ACC-22则无此作用。AAC-22与脾细胞的结合与ACC-22并无差异。将AAC-22脂质转染至脾细胞可显著增强IFN的产生和NK细胞活性，而ACC-22的脂质转染则几乎没有增强作用。这些结果有力地表明，IFN产生的前提条件不是AAC-22与细胞表面受体的结合，而是其渗透到脾细胞中。
