Watson S R, Collins F M
Immunology. 1980 Mar;39(3):367-73.
Specific pathogen-free B6D2 mice were infected intravenously with 10(8) viable BCG, M. habana or M. simiae and the level of tuberculin hypersensitivity to 2.5 micrograms PPD or cytoplasmic protein antigens (CPA) prepared from the other organisms was determined using the footpad swelling test with increasing time after infection. This was correlated with the growth or persistence of mycobacterial populations within the liver. Spleen cells were removed from these infected mice and the level of blast transformation following exposure to PHA, PPD or M. habana or M. simiae CPA was measured in vitro. Early in the mycobacterial infections (day 14) thymidine incorporation by the spleen cells was significantly enchanced followed by a profound depression in incorporation rates as the infection progressed. The mechanism of this depressed response involved the production of suppressor T cells in the spleen. In the case of the M. simiae or M. habana infection, cells capable of mediating suppression were still present even after 12 months of infection. In the BCG infection, suppressor T cells declined with time so that by 4 months incorporation rates were back to normal and suppressor cells were no longer detectable in the spleens of the infected animals.
将10⁸个活的卡介苗、哈氏分枝杆菌或猿分枝杆菌经静脉注射感染无特定病原体的B6D2小鼠，并在感染后随时间增加，使用足垫肿胀试验测定对2.5微克结核菌素纯蛋白衍生物（PPD）或由其他生物体制备的细胞质蛋白抗原（CPA）的结核菌素超敏反应水平。这与肝脏内分枝杆菌群体的生长或持续存在相关。从这些感染小鼠中取出脾细胞，并在体外测量暴露于PHA、PPD或哈氏分枝杆菌或猿分枝杆菌CPA后母细胞转化的水平。在分枝杆菌感染早期（第14天），脾细胞的胸苷掺入显著增强，随后随着感染进展掺入率大幅下降。这种反应抑制的机制涉及脾中抑制性T细胞的产生。在猿分枝杆菌或哈氏分枝杆菌感染的情况下，即使在感染12个月后仍存在能够介导抑制作用的细胞。在卡介苗感染中，抑制性T细胞随时间下降，以至于到4个月时掺入率恢复正常，并且在感染动物的脾脏中不再检测到抑制细胞。
