Majlessi L, Benaroch P, Bordenave G
Unité d'Immunophysiologie Moléculaire, Institut Pasteur, Paris, France.
J Immunol. 1992 Sep 15;149(6):1881-8.
One of the problems raised by the T cell-induced allotypic suppression is the origin (donor or host) of the T cells responsible for the chronicity of the suppression. To address this point, we used T cells from Igha/a Thy-1.2 mice whose natural T cell activity against IgG2ab was enhanced in vivo. These T cells were injected into newborn Ighb/b Thy-1.1 mice where they induced complete suppression of IgG2ab expression in around 70% of these recipients. During a study that lasted more than 1 yr, we found that about 3% of the recipient splenocytes were T cells of the donor type. By means of suppression-transfer experiments, using either Thy-1.2+ or Thy-1.1+ cell-depleted splenocytes from mice suppressed in this manner we were able to unambiguously show that Thy-1.2+ cell-depleted splenocytes were incapable of transferring the suppression, whereas Thy-1.1+ cell-depleted splenocytes could. We thus demonstrated that suppression was maintained throughout the recipient's life by donor Thy-1.2+ T cells.
T细胞诱导的同种异型抑制所引发的问题之一是，负责抑制持续性的T细胞的来源（供体或宿主）。为了解决这一问题，我们使用了来自Igha/a Thy-1.2小鼠的T细胞，这些小鼠针对IgG2ab的天然T细胞活性在体内得到增强。将这些T细胞注射到新生的Ighb/b Thy-1.1小鼠体内，在约70%的这些受体小鼠中诱导了IgG2ab表达的完全抑制。在一项持续超过1年的研究中，我们发现约3%的受体脾细胞是供体类型的T细胞。通过抑制转移实验，使用以此种方式受到抑制的小鼠的Thy-1.2+或Thy-1.1+细胞耗竭的脾细胞，我们能够明确表明，Thy-1.2+细胞耗竭的脾细胞无法转移抑制作用，而Thy-1.1+细胞耗竭的脾细胞可以。因此，我们证明抑制作用在受体的整个生命过程中由供体Thy-1.2+ T细胞维持。
