Jokiph L
Immunology. 1973 Aug;25(2):283-95.
The migration of peritoneal exudate cells (PEC) from rats with delayed skin reactivity to diphtheria toxoid (DT) and tuberculin (PPD) was inhibited in the presence of antigen. Three days after an intravenous injection of 2.5 mg of DT there was no inhibition with DT. Seven and 28 days later migration was inhibited but less than in sensitized controls. In 6 weeks the difference disappeared. Three days after the DT challenge, the migration inhibition with PPD was weaker than in the sensitized controls. From day 7 on, non-specific reduction of migration inhibition was not detected. The 24-hour skin reactivity to DT and PPD closely paralleled the phenomena. The mechanism of desensitization appears to be the lack or a functional defect of the specific cells or a blocking factor unremovable by washing or produced during the migration assay.
在抗原存在的情况下,对白喉类毒素(DT)和结核菌素(PPD)皮肤迟发性反应大鼠的腹腔渗出细胞(PEC)迁移受到抑制。静脉注射2.5mg DT三天后,DT对迁移没有抑制作用。7天和28天后迁移受到抑制,但程度低于致敏对照组。6周后差异消失。DT激发三天后,PPD对迁移的抑制作用弱于致敏对照组。从第7天起,未检测到迁移抑制的非特异性降低。对DT和PPD的24小时皮肤反应与这些现象密切平行。脱敏机制似乎是特异性细胞缺乏或存在功能缺陷,或者是一种无法通过洗涤去除或在迁移试验过程中产生的阻断因子。