Tarcic N, Baler R, Naor D
Scand J Immunol. 1984 Nov;20(5):389-401. doi: 10.1111/j.1365-3083.1984.tb01018.x.
X-irradiated (250 rad), cyclophosphamide-treated or ATx A mice injected with syngeneic trinitrophenylated spleen cells (TNP-SC) and footpad challenged with syngeneic lymphoblasts generated delayed-type hypersensitivity (DTH) responses 24, 48 and 72 h after challenge. The syngeneic-DTH (syn-DTH) response was mediated by Lyt-1+ cells and suppressed with Lyt-1+2+3+, I-Jk+ cells. The suppressor cells were obtained from spleens or thymuses of normal syngeneic mice. Suppressor factor (SF) was extracted or released from Lyt-1+2+3+, I-Jk+ cells obtained from normal A mice (but not from X-irradiated A mice). The factor blocked the DTH responses of X-irradiated mice injected with syngeneic TNP-SC and challenged with syngeneic lymphoblasts when injected into the mice both at the induction phase and the elicitation phase of the DTH. The factor failed to abrogate allogeneic and xenogeneic DTH. However, allogeneic factor (derived from C57BL/6 mice) abolished the syn-DTH response of mice injected with syngeneic TNP-SC and challenged with syngeneic lymphoblasts. The SF was produced by Lyt-1+2+3+, I-Jk+ T cells or by thymocytes. The combined extracted product of Lyt-1+ and Lyt-2+ cells did not abrogate the syn-DTH response. Normal spleen cells depleted of phagocytes by a magnetic procedure also produced the SF. These findings indicate, therefore, that suppressive factor (or factors; see Discussion in the accompanying paper, Ref. 17) controls the immunological autoreactivity against syngeneic TNP-SC.
用250拉德X射线照射、环磷酰胺处理或注射同基因三硝基苯化脾细胞(TNP-SC)的ATx A小鼠,并用同基因成淋巴细胞攻击足垫,在攻击后24、48和72小时产生迟发型超敏反应(DTH)。同基因DTH(syn-DTH)反应由Lyt-1+细胞介导,并被Lyt-1+2+3+、I-Jk+细胞抑制。抑制细胞取自正常同基因小鼠的脾脏或胸腺。抑制因子(SF)从正常A小鼠(而非X射线照射的A小鼠)获得的Lyt-1+2+3+、I-Jk+细胞中提取或释放。该因子在DTH的诱导期和激发期注入小鼠时,可阻断注射同基因TNP-SC并用同基因成淋巴细胞攻击的X射线照射小鼠的DTH反应。该因子未能消除同种异体和异种DTH。然而,同种异体因子(源自C57BL/6小鼠)消除了注射同基因TNP-SC并用同基因成淋巴细胞攻击的小鼠的syn-DTH反应。SF由Lyt-1+2+3+、I-Jk+ T细胞或胸腺细胞产生。Lyt-1+和Lyt-2+细胞的联合提取物不能消除syn-DTH反应。通过磁性程序去除吞噬细胞的正常脾细胞也产生SF。因此,这些发现表明,抑制因子(或多种因子;见随附论文的讨论,参考文献17)控制针对同基因TNP-SC的免疫自身反应性。