Manson J, Brown T, Duff G
AFRC and MRC Neuropathogenesis Unit, Edinburgh, Scotland.
Lymphokine Res. 1990 Spring;9(1):35-42.
The production of interleukin 1 beta (IL1 beta) in lipopolysaccharide (LPS) stimulated monocytes was inhibited by 98% using antisense phosphorothioate oligonucleotides complementary to the 5' untranslated and exon 6 regions of IL1 beta mRNA. A sense phosphorothioate oligonucleotide failed to inhibit IL1 beta production. The inhibition of IL1 beta synthesis was not due to reduced cell viability and [35S]methionine incorporation showed that it could not be accounted for by an overall inhibition in protein synthesis. Tumour necrosis factor (TNF) and IL1 alpha production was also inhibited but to a lesser extent than IL1 beta. The use of antisense phosphorothioate oligonucleotides to inhibit IL1 production should enable the complex pathways of IL1 regulation to be elucidated and provide information on the biological role of these cytokines.
使用与白细胞介素1β（IL1β）mRNA的5'非翻译区和第6外显子区域互补的反义硫代磷酸酯寡核苷酸，脂多糖（LPS）刺激的单核细胞中IL1β的产生被抑制了98%。正义硫代磷酸酯寡核苷酸未能抑制IL1β的产生。IL1β合成的抑制并非由于细胞活力降低，并且[35S]甲硫氨酸掺入表明其不能由蛋白质合成的全面抑制来解释。肿瘤坏死因子（TNF）和IL1α的产生也受到抑制，但程度小于IL1β。使用反义硫代磷酸酯寡核苷酸抑制IL1的产生应能阐明IL1调节的复杂途径，并提供有关这些细胞因子生物学作用的信息。
