Knudsen T E, Larsen C S, Johnsen H E
Scand J Immunol. 1987 May;25(5):527-31. doi: 10.1111/j.1365-3083.1987.tb02224.x.
Interleukin 2 (IL-2) was shown to induce a small but significant increase in the level of cGMP after 20 min stimulation and a subsequent fall after 1 h in activated T lymphocytes. No change in the level of cAMP was observed. Addition of the cyclic nucleotide analogues dbcAMP or dbcGMP did not stimulate DNA synthesis. On the contrary, IL-2-induced [3H]thymidine incorporation was inhibited by these drugs. Further, the phosphodiesterase inhibitor theophylline inhibited proliferation of activated T lymphocytes. Our results indicate that neither cAMP nor cGMP act as 'second messengers' for IL-2 but support the theory that cAMP is a negative regulator of cell proliferation.
白细胞介素2（IL-2）在激活的T淋巴细胞中刺激20分钟后可使环磷酸鸟苷（cGMP）水平有小幅但显著的升高，1小时后则随之下降。未观察到环磷酸腺苷（cAMP）水平有变化。添加环核苷酸类似物双丁酰环磷腺苷（dbcAMP）或双丁酰环磷鸟苷（dbcGMP）不会刺激DNA合成。相反，这些药物抑制了IL-2诱导的[3H]胸腺嘧啶核苷掺入。此外，磷酸二酯酶抑制剂茶碱抑制了激活的T淋巴细胞的增殖。我们的结果表明，cAMP和cGMP均不作为IL-2的“第二信使”，但支持cAMP是细胞增殖负调节因子这一理论。
