Orme I M, Collins F M
Infect Immun. 1984 Jan;43(1):32-7. doi: 10.1128/iai.43.1.32-37.1984.
The results of in vitro experiments designed to measure the immunocompetence of mice heavily infected with the atypical mycobacterial pathogens Mycobacterium avium and Mycobacterium simiae were compared with the results of experiments which used in vivo approaches. Blastogenic responsiveness in vitro both to mitogen and to alloantigen was severely depressed in the heavily infected mice; this responsiveness could be restored by removal of an inhibitory Thy-1.2-, nylon wool-adherent cell population. No evidence was found to support the previous contention that suppressor T cells may play a role in the inhibition of this responsiveness. These results were then compared with experiments which measured the ability of the infected animal to elicit a delayed-type hypersensitivity response to sheep erythrocytes in vivo. However, although delayed-type hypersensitivity responses in vivo were also depressed, evidence was obtained which suggested that this unresponsiveness was due to inadequate sensitization of T cells, possibly due to catabolism of antigen, rather than due to the influence of an active, immunosuppressive mechanism. Finally, despite the severely depressed ability of cells from infected mice to respond to alloantigenic stimulation in vitro, infected animals were fully able to cause the regression of a tumor implant in vivo.
将旨在测量重度感染非典型分枝杆菌病原体鸟分枝杆菌和猿分枝杆菌的小鼠免疫能力的体外实验结果,与采用体内方法的实验结果进行了比较。在重度感染的小鼠中,体外对丝裂原和同种异体抗原的增殖反应性严重降低;通过去除抑制性的Thy-1.2阳性、尼龙毛粘附细胞群体,这种反应性可以恢复。没有发现证据支持先前关于抑制性T细胞可能在抑制这种反应性中起作用的论点。然后将这些结果与测量感染动物在体内对绵羊红细胞引发迟发型超敏反应能力的实验进行了比较。然而,尽管体内迟发型超敏反应也受到抑制,但获得的证据表明,这种无反应性是由于T细胞致敏不足,可能是由于抗原分解代谢,而不是由于活跃的免疫抑制机制的影响。最后,尽管感染小鼠的细胞在体外对同种异体抗原刺激的反应能力严重降低,但感染动物在体内完全能够使肿瘤移植物消退。