Strom T B, Carpenter C B, Garovoy M R, Austen K F, Merrill J P, Kaliner M
J Exp Med. 1973 Aug 1;138(2):381-93. doi: 10.1084/jem.138.2.381.
The capacity of allosensitized thymus-derived lymphocytes to destroy target cells bearing donor alloantigens is modulated by the cellular levels of cyclic AMP and cyclic GMP. Increases in the cyclic AMP levels of attacking lymphocytes by stimulation with prostaglandin E(1), isoproterenol, and cholera toxin inhibit lymphocyte-mediated cytotoxicity; whereas, depletion of cyclic AMP with imidazole enhances cytotoxicity. The augmentation of cytotoxicity produced by cholinergic stimulation with carbamylcholine is not associated with alterations in cyclic AMP levels and is duplicated by 8-bromo-cyclic GMP. The effects of activators of adenylate cyclase, cholinomimetic agents, and 8-bromocyclic GMP are upon the attacking and not the target cells and occur at the time of initial interaction of attacking and target cells. Indeed, the level of cyclic nucleotide (cyclic AMP and cyclic GMP) at the time of initial cell-to-cell interaction determines the extent of cytotoxicity.
同种致敏的胸腺衍生淋巴细胞破坏带有供体同种异体抗原的靶细胞的能力受环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）细胞水平的调节。通过前列腺素E（1）、异丙肾上腺素和霍乱毒素刺激来提高攻击淋巴细胞的cAMP水平会抑制淋巴细胞介导的细胞毒性；而用咪唑消耗cAMP则会增强细胞毒性。氨甲酰胆碱胆碱能刺激所产生的细胞毒性增强与cAMP水平的改变无关，且可被8-溴环鸟苷复制。腺苷酸环化酶激活剂、拟胆碱剂和8-溴环鸟苷的作用是作用于攻击细胞而非靶细胞，且发生在攻击细胞与靶细胞初始相互作用之时。实际上，初始细胞间相互作用时的环核苷酸（cAMP和cGMP）水平决定了细胞毒性的程度。
