Kondratyeva T K, Fontalin L N, Mikheeva N V
Gamaleya Institute for Epidemiology and Microbiology, Academy of Medical Sciences, Moscow, Russia.
Immunol Lett. 1992 Sep;34(1):71-7. doi: 10.1016/0165-2478(92)90029-n.
In the murine system in vivo administration of several T-cell mitogens (LcA, Con A, anti-Thy 1.2 mAb) followed by cyclophosphamide (CP) inhibited the functional activity of T-cell subsets (Th1, Th2, Ts) but not that of B cells. T-cell counts in the spleen of treated mice proved to be significantly decreased. Conversely, T mitogens or CP alone produced a negligible effect if any. Adoptively transferred thymocytes from intact donors restored T-dependent splenocyte responses in experimental mice. In addition, it did not suppress the normal response to sheep red blood cells (SRBC). Our results indicated that the acquired immune deficiency under study is caused by polyclonal elimination (deletion) of mitogen-stimulated T cells, and could be regarded as a model of CP-induced tolerance.
在小鼠体内系统中，给小鼠注射几种T细胞丝裂原（脂多糖、刀豆蛋白A、抗Thy 1.2单克隆抗体），随后注射环磷酰胺，可抑制T细胞亚群（Th1、Th2、Ts）的功能活性，但不影响B细胞的功能活性。经处理的小鼠脾脏中的T细胞计数显著降低。相反，单独使用T丝裂原或环磷酰胺即使有作用也微乎其微。从完整供体过继转移的胸腺细胞可恢复实验小鼠中依赖T细胞的脾细胞反应。此外，它并不抑制对绵羊红细胞（SRBC）的正常反应。我们的结果表明，所研究的获得性免疫缺陷是由丝裂原刺激的T细胞的多克隆消除（缺失）引起的，可被视为环磷酰胺诱导的耐受模型。
