Rouveix B, Larno S, Badenoch-Jones P, Lechat P
Agents Actions. 1981 Dec;11(6-7):622-4. doi: 10.1007/BF01978767.
Human lymphokine (LK) is known to induce guinea pig macrophage aggregation. This effect can be quantitatively measured with a Born modified platelet aggregometer. This method has been well correlated with the state of delayed hypersensitivity. Previous findings about the mechanism of action of the aggregation indicated that this aggregation is not due to an increase in the cellular level of c-AMP. It is doubtful whether c-AMP is a messenger of the LK action. Using a radio-immunoassay, small but significant increases were found in c-GMP levels of LK-aggregated macrophages. In addition, exogenous dibutyryl c-GMP and carbamylcholine induced a macrophage aggregation, as did the divalent cation ionophore A-23187. These data, together with the fact that LK-induced macrophage aggregation is inhibited by colchicine and at 0 degree C, suggest that microtubule polymerization is involved in this process.
已知人类淋巴因子（LK）可诱导豚鼠巨噬细胞聚集。这种效应可用改良的博恩血小板聚集仪进行定量测量。该方法与迟发型超敏反应状态密切相关。先前关于聚集作用机制的研究结果表明，这种聚集并非由于细胞内c - AMP水平升高所致。c - AMP是否为LK作用的信使尚不确定。通过放射免疫测定发现，LK聚集的巨噬细胞中c - GMP水平有小幅但显著的升高。此外，外源性二丁酰c - GMP和氨甲酰胆碱可诱导巨噬细胞聚集，二价阳离子载体A - 23187也有此作用。这些数据，连同秋水仙碱和在0摄氏度时LK诱导的巨噬细胞聚集受到抑制这一事实，表明微管聚合参与了这一过程。
