Phillips S M, Zweiman B
J Exp Med. 1973 Jun 1;137(6):1494-510. doi: 10.1084/jem.137.6.1494.
The mechanism of suppression, of delayed hypersensitivity to tuberculoprotein by 6-mercaptopurine (6-MP) was studied in guinea pigs. Under the conditions of the protocol, suppression of tuberculin delayed skin test reactivity was not associated with a significantly altered end-organ response to mediators of permeability. No significant alteration of in vivo lymphoid activity, as measured by reconstitution studies, was found. In addition, lymphoid cells from 6-MP-treated animals reacted in a fashion similar to those of placebo-treated animals with respect to (a) antigen-induced lymphocyte proliferation, (b) antigen-induced liberation of macrophage inhibitory factor activity, (c) direct inhibition by antigen of peritoneal exudate cell migration. Conversely, suppression was seen in levels of blood monocytes and in vitro function of macrophages from 6-MP-treated animals in several respects: (a) adherence to glass, (b) migratory rate, (c) phagocytic capacity. Therefore, it would appear that a ma]or mechanism of 6-MP-induced suppression of delayed hypersensitivity is through its action on effector cells.
在豚鼠中研究了6-巯基嘌呤（6-MP）抑制对结核蛋白迟发型超敏反应的机制。在该实验方案的条件下，结核菌素迟发型皮肤试验反应性的抑制与对通透性介质的终末器官反应的显著改变无关。通过重建研究测定，未发现体内淋巴活性有显著改变。此外，来自6-MP处理动物的淋巴细胞在以下方面的反应方式与安慰剂处理动物的相似：（a）抗原诱导的淋巴细胞增殖，（b）抗原诱导的巨噬细胞抑制因子活性的释放，（c）抗原对腹腔渗出细胞迁移的直接抑制。相反，在几个方面观察到6-MP处理动物的血液单核细胞水平和巨噬细胞的体外功能受到抑制：（a）对玻璃的粘附，（b）迁移率，（c）吞噬能力。因此，6-MP诱导迟发型超敏反应抑制的主要机制似乎是通过其对效应细胞的作用。
