Voitenok N N, Misuno N I, Panyutich A V, Kolesnikova T S
Institute of Experimental Hematology and Biotechnology, All-Union Scientific Center of Hematology, Moscow, U.S.S.R.
Immunol Lett. 1989 Jan 15;20(1):77-82. doi: 10.1016/0165-2478(89)90072-2.
Human blood monocytes and lymphocytes were separated by Percoll gradient fractionation. The synthesis of RNA was inhibited by actinomycin D (AcD) or alpha-amanitin (Amn). Monocytes were stimulated with LPS, lymphocytes were stimulated with phytohaemagglutinin (PHA). The activity of tumor necrosis factor (TNF-alpha) and lymphotoxin (LT) was measured by L-929 cell assay. It was shown that induction of TNF-alpha synthesis by LPS was not blocked by AcD and Amn. In contrast, the production of LT was blocked in cultures of lymphocytes treated by the inhibitors. Moreover, TNF-alpha synthesis was induced in resting monocyte cultures by AcD. Cycloheximide (Cy) inhibited the production of TNF-alpha. The data imply that TNF-alpha synthesis by human blood monocytes can be induced by posttranscriptional regulation of TNF-alpha mRNA presynthesized in vivo.
通过Percoll梯度分级分离人血单核细胞和淋巴细胞。用放线菌素D（AcD）或α-鹅膏蕈碱（Amn）抑制RNA的合成。用脂多糖（LPS）刺激单核细胞，用植物血凝素（PHA）刺激淋巴细胞。通过L-929细胞测定法测量肿瘤坏死因子（TNF-α）和淋巴毒素（LT）的活性。结果表明，LPS诱导的TNF-α合成不受AcD和Amn的阻断。相反，在经抑制剂处理的淋巴细胞培养物中，LT的产生受到阻断。此外，AcD在静息单核细胞培养物中诱导TNF-α合成。放线菌酮（Cy）抑制TNF-α的产生。这些数据表明，人血单核细胞中TNF-α的合成可通过体内预先合成的TNF-α mRNA的转录后调控来诱导。
