Schreiner G F, Unanue E R
J Immunol. 1975 Feb;114(2 pt 2):802-8.
Translational movement in B lymphocytes was stimulated by anti-Ig antibody. Drugs that are presumed to elevate cyclic AMP stopped this stimulated motility. Such was the case with dibutyryl cAMP and theophylline, cholera enterotoxin, and isoproterenol, a beta adrenergic agonist. Conversely, in the absence of anti-immunoglobulin antibody, cyclic GMP and the cholinergic drugs acetylcholine and carbamylcholine increased spontaneous motility of lymphocytes, with the B class of lymphocytes demonstrating greater responsiveness. The increase in motility brought about by cholinergic drugs was totally stopped by atropine, suggesting that the B lymphocyte surface contains a cholinergic receptor. The inhibition of anti-immunoglobulin-stimulated movement produced by cyclic AMP was not observed if the cells were first incubated with colchicine, the microtubular-disrupting drug. This suggests that the cyclic AMP-decreased motility was brought about by the increased stabilization of microtubules. Lymphocyte motility was dissociable from other early events subsequent to binding of anti-immunoglobulin antibodies: patching, capping, and endocytosis of complexes were unaffected by cyclic AMP, cyclic GMP, or drugs of the adrenergic or cholinergic systems.
抗 Ig 抗体刺激 B 淋巴细胞的平移运动。据推测能提高环磷酸腺苷（cAMP）水平的药物可阻止这种受刺激的运动。二丁酰 cAMP、茶碱、霍乱肠毒素以及β肾上腺素能激动剂异丙肾上腺素就是这样的情况。相反，在没有抗免疫球蛋白抗体的情况下，环磷酸鸟苷（cGMP）以及胆碱能药物乙酰胆碱和氨甲酰胆碱会增加淋巴细胞的自发运动，其中 B 类淋巴细胞表现出更高的反应性。胆碱能药物引起的运动增加被阿托品完全阻断，这表明 B 淋巴细胞表面含有胆碱能受体。如果细胞先用秋水仙碱（一种破坏微管的药物）孵育，就不会观察到环磷酸腺苷对抗免疫球蛋白刺激的运动的抑制作用。这表明环磷酸腺苷降低的运动是由微管稳定性增加导致的。淋巴细胞运动与抗免疫球蛋白抗体结合后的其他早期事件可分离：复合物的贴片、帽化和内吞作用不受环磷酸腺苷、环磷酸鸟苷或肾上腺素能或胆碱能系统药物的影响。
