Jakschik B A, Rengers T A, Pinski J R
Washington University School of Medicine, Department of Pharmacology, St. Louis, Missouri 63110.
Adv Prostaglandin Thromboxane Leukot Res. 1987;17A:180-5.
The experiments discussed above indicate that during immediate hypersensitivity reactions, macrophages are stimulated by mast cells to synthesize PGE2 and 6-keto-PGF1 alpha but not LTC4. The arachidonic acid utilized for these products is mobilized from the macrophages itself and not shuttled from the mast cells. The stimulus for the involvement of the macrophage does not appear to be a direct cell interaction between the two cell types or a soluble factor released by the mast cells. Since the profile of eicosanoids produced by macrophages when exposed to mast cell granules is similar to that observed in the contribution of macrophages to immediate hypersensitivity reactions, mast cell granules appear to be responsible for the recruitment of macrophages to this reaction.
上述讨论的实验表明，在速发型超敏反应期间，肥大细胞刺激巨噬细胞合成前列腺素E2（PGE2）和6-酮-前列腺素F1α（6-keto-PGF1 alpha），但不合成白三烯C4（LTC4）。用于这些产物合成的花生四烯酸是从巨噬细胞自身动员而来的，并非由肥大细胞转运而来。巨噬细胞参与反应的刺激因素似乎不是两种细胞类型之间的直接细胞相互作用，也不是肥大细胞释放的可溶性因子。由于巨噬细胞在接触肥大细胞颗粒时产生的类花生酸谱与巨噬细胞在速发型超敏反应中的作用所观察到的相似，肥大细胞颗粒似乎负责将巨噬细胞招募到该反应中。
