Jayaraman S, Bellone C J
Cell Immunol. 1986 Sep;101(2):351-62. doi: 10.1016/0008-8749(86)90148-6.
Previous studies demonstrated that the first-order T-suppressor factor (TsF1) requires the presence of antigen to induce idiotype-specific Ts cells which readily suppress phenyltrimethylamino (TMA) hapten-specific delayed-type hypersensitivity (DTH) responses when transferred into already immune recipients. In this study we show that TsF1 in the absence of antigen induces a splenic population which limits DTH in recipient mice only when an additional accessory lymphoid population was also cotransferred. Neither of these populations alone was sufficient to mediate suppression and depletion of T cells in either population's abrogated suppression, indicating the T-cell dependency of the complementing cell types. Moreover, suppression was seen only when TMA-TsF1-induced and not normal spleen cell lysate-induced cells were cotransferred with the antigen-induced population, suggesting the requirement for a specific signal to induce the factor-induced population. Further experiments showed that the antigen-induced lymphoid population could be replaced by either heterologous antigen-induced or adjuvant alone-induced splenic populations, indicating the lack of specificity of this secondary population. Further analysis showed that the cell complementation between TMA-TsF1-induced and the nonspecific accessory lymphoid population resulted in antigen-specific and genetically restricted immune suppression. The TsF1-induced lymphoid population was not responsible for the genetic restriction, and furthermore, there was no restriction observed between the two complementing populations. However, matching of the nonspecific accessory cell with the recipient host at the I-J subregion of the H-2 complex was essential for immune suppression. Finally, the activity of complementing cells was found to be independent of cyclophosphamide-sensitive Ts populations of the recipient mice. The ramifications of these findings with reference to the existing suppressor pathways are discussed.
先前的研究表明，一级T抑制因子（TsF1）需要有抗原存在才能诱导独特型特异性Ts细胞，当将这些细胞转移到已经免疫的受体中时，它们能轻易抑制苯三甲基氨基（TMA）半抗原特异性迟发型超敏反应（DTH）。在本研究中，我们发现，在没有抗原的情况下，TsF1诱导的脾脏细胞群体只有在同时共转移另外一个辅助性淋巴细胞群体时，才会限制受体小鼠的DTH反应。单独的这两个群体都不足以介导抑制作用，并且去除任一群体中的T细胞都会废除抑制作用，这表明互补细胞类型对T细胞具有依赖性。此外，只有当TMA - TsF1诱导的细胞而非正常脾细胞裂解物诱导的细胞与抗原诱导的细胞群体共转移时，才会出现抑制作用，这表明需要特定信号来诱导因子诱导的细胞群体。进一步的实验表明，抗原诱导的淋巴细胞群体可以被异源抗原诱导的或单独佐剂诱导的脾脏细胞群体所取代，这表明该二级细胞群体缺乏特异性。进一步分析表明，TMA - TsF1诱导的细胞群体与非特异性辅助淋巴细胞群体之间的细胞互补作用导致了抗原特异性和基因限制性免疫抑制。TsF1诱导的淋巴细胞群体与基因限制无关，此外，在两个互补群体之间未观察到限制作用。然而，非特异性辅助细胞与受体宿主在H - 2复合体的I - J亚区的匹配对于免疫抑制至关重要。最后，发现互补细胞的活性与受体小鼠对环磷酰胺敏感的Ts群体无关。讨论了这些发现对现有抑制途径的影响。
