Butler L D, Battisto J R
Ann N Y Acad Sci. 1979;332:524-30. doi: 10.1111/j.1749-6632.1979.tb47146.x.
We have extended our studies which show that hapten-specific killer T-cells can be generated in vivo towards hapten-conjugated, syngeneic spleen cells provided an auxiliary antigenic stimulus is incorporated. M1s antigen served in this auxiliary capacity by stimulating helper T-cells. Natural or experimental tolerance to these antigens abrogated cytotoxicity. Effecting tolerance in host animals towards target hapten also prevented development of the genetically restricted killer T-cells. Thus, cytolytic T-cells can be controlled equally at the levels of helper and pre-killer cells. While adoptive transfer of hapten-specific tolerance by means of spleen cells did not abrogate appearance of hapten-specific killer T-cells, it did prevent hapten-specific DTH. Thus, the mechanism for regulating the latter may differ significantly from that for CML.
我们扩展了研究,结果表明,如果引入辅助抗原刺激,针对半抗原结合的同基因脾细胞,体内可产生半抗原特异性杀伤性T细胞。M1s抗原通过刺激辅助性T细胞发挥这种辅助作用。对这些抗原的天然或实验性耐受性消除了细胞毒性。使宿主动物对靶半抗原产生耐受性也阻止了基因限制性杀伤性T细胞的发育。因此,细胞溶解性T细胞在辅助细胞和前杀伤细胞水平上均可得到同等控制。虽然通过脾细胞进行半抗原特异性耐受性的过继转移并没有消除半抗原特异性杀伤性T细胞的出现,但它确实阻止了半抗原特异性迟发型超敏反应。因此,调节后者的机制可能与调节慢性粒细胞白血病的机制有显著差异。