Hodes R J, Hathcock K S
J Immunol. 1976 Jan;116(1):167-77.
It was observed that when normal mouse spleen cells were cultured alone in vitro (precultured) for 3 to 7 days, these cells lost the ability to generate cell-mediated cytotoxicity (CML) during subsequent in vitro sensitization with allogeneic spleen cells, trinitrophenyl (TNP)-modified syngeneic spleen cells, or syngeneic tumor cells. These precultured cells, which were themselves unable to generate CML, were also shown in mixing experiments to suppress, actively, the generation of CML by freshly explanted spleen cells. Suppression occurred at the sensitization phase of CML, and not at the effector level; supernatants from suppressive precultured cells were not suppressive. Suppression was totally abrogated by the treatment of spleen cells with a T cell-specific rabbit anti-mouse brain serum and complement (RalphaMB+C) either before or after preculturing, suggesting that a T cell eas essential both to the generation of suppressor activity and to its expression. Suppressor activity was entirely absent in precultured nylon wool column-nonadherent spleen cells, a T cell-enriched population containing most of the RalphaMB+C-sensitive cells in the spleen. Precultured nylon column-adherent cells (T cell-depleted) did have suppressive activity, and a mixture of nylon-adherent and nylon-non-adherent cells was a suppressive after preculture as the precultured unseparated spleen. Moreover, the ability of nylon-adherent spleen cells to generate suppressive activity during preculturing was abrogated by treatment with RalphaMB+C. Thus, the "spontaneous" generation of CML-suppressive activity was dependent upon a limited subpopulation of splenic T cells isolated in the nylon column-adherent fraction. The relationship of these data to a previously described synergy between subpopulations of normal spleen in the generation of CML is discussed, and the findings related to other suppressor systems described in the literature.
据观察，当正常小鼠脾细胞在体外单独培养（预培养）3至7天时，这些细胞在随后用同种异体脾细胞、三硝基苯基（TNP）修饰的同基因脾细胞或同基因肿瘤细胞进行体外致敏过程中，失去了产生细胞介导细胞毒性（CML）的能力。这些预培养的细胞自身无法产生CML，在混合实验中还显示，它们能积极抑制新鲜分离的脾细胞产生CML。抑制发生在CML的致敏阶段，而非效应阶段；抑制性预培养细胞的上清液无抑制作用。在用T细胞特异性兔抗小鼠脑血清和补体（RalphaMB + C）处理脾细胞后，无论是在预培养之前还是之后，抑制作用都完全消除，这表明T细胞对于抑制活性的产生及其表达均至关重要。预培养的尼龙毛柱非黏附脾细胞中完全没有抑制活性，该细胞群体富含T细胞，包含脾中大多数对RalphaMB + C敏感的细胞。预培养的尼龙柱黏附细胞（T细胞耗竭）确实具有抑制活性，尼龙黏附细胞和尼龙非黏附细胞的混合物在预培养后与未分离的预培养脾细胞一样具有抑制作用。此外，用RalphaMB + C处理后，尼龙黏附脾细胞在预培养期间产生抑制活性的能力被消除。因此，CML抑制活性的“自发”产生依赖于在尼龙柱黏附部分中分离出的有限脾T细胞亚群。讨论了这些数据与先前描述的正常脾亚群在CML产生过程中的协同作用之间的关系，并将这些发现与文献中描述的其他抑制系统相关联。
