Ferguson T A, Hayashi J D, Kaplan H J
Department of Ophthalmology, Washington University School of Medicine, St. Louis, MO 63110.
J Immunol. 1989 Aug 1;143(3):821-6.
After the anterior chamber (AC) injection of trinitrophenol-coupled (TNP) spleen cells, it is observed that systemic delayed-type hypersensitivity responses to TNP are inhibited by Ag-specific suppressor T cells. We recently reported that suppression is initiated by viable TNP-coupled T cells within the inoculum and upon further analysis we found that these cells have the surface phenotype of CD4+ Ts inducer cells. We report here that treatment of these TNP-T cells with cycloheximide or cytochalasin-B before to AC injection abolishes suppression, whereas treatment with 2000 rad radiation does not. This indicates that protein synthesis and secretion are required to initiate suppression but proliferation is not. Further, we demonstrate the adoptive transfer of suppression by serum of AC inoculated animals. Detection of the component in serum in adoptive transfer assays, however, requires removal of the spleen before AC injection. We establish that the material in serum is a Ts cell product (T suppressor-inducer factor) based on three criteria: it is Ag specific, genetically restricted, and reactive with a mAb that specifically identifies these molecules. These results suggest that the signal leaving the eye to induce suppression of delayed-type hypersensitivity is T cell derived and that molecules mediating immune regulation for this organ are made within the eye and transported via the serum to the spleen.
在前房（AC）注射三硝基苯酚偶联（TNP）的脾细胞后，观察到对TNP的全身性迟发型超敏反应受到抗原特异性抑制性T细胞的抑制。我们最近报道，抑制作用由接种物中存活的TNP偶联T细胞启动，进一步分析发现这些细胞具有CD4 + Ts诱导细胞的表面表型。我们在此报告，在AC注射前用环己酰亚胺或细胞松弛素B处理这些TNP-T细胞可消除抑制作用，而用2000拉德辐射处理则不会。这表明蛋白质合成和分泌是启动抑制作用所必需的，但增殖不是。此外，我们证明了AC接种动物血清中抑制作用的过继转移。然而，在过继转移试验中检测血清中的成分需要在AC注射前切除脾脏。基于三个标准，我们确定血清中的物质是一种Ts细胞产物（T抑制诱导因子）：它是抗原特异性的、基因受限的，并且与特异性识别这些分子的单克隆抗体反应。这些结果表明，离开眼睛以诱导迟发型超敏反应抑制的信号是T细胞衍生而来的，并且介导该器官免疫调节的分子在眼内产生并通过血清转运至脾脏。
