Johnston M F, Slavin R G
J Lab Clin Med. 1976 Mar;87(3):457-61.
Cell-mediated immunity is reduced in uremia, but the mechanism of this inhibition is poorly understood. To determine the site of inhibition a study of adoptive transfer of cell-mediated immunity was undertaken. Strain 13 guinea pigs were made uremic by ureteral ligation. Lymph node cells were isolated and transferred in the following three ways: Group 1: tuberculin sensitive nonuremic donors to nonimmune nonuremic recipients; Group 2: tuberculin sensitive nonuremic donors to nonimmune uremic recipients; Group 3: tuberculin sensitive uremic donors to nonimmune nonuremic recipients. There was no difference in the skin test responses of the transfer recipients in Groups 1 and 3, even though the uremic donors in Group 3 had lost their skin test reactivity. Transfer of tuberculin sensitivity was not successful in Group 2. These results indicate that the uremic state inhibits previously established skin test reactivity but does not prevent sensitized T lymphocytes from transferring cellular immunity.
尿毒症患者的细胞介导免疫功能降低，但其抑制机制尚不清楚。为了确定抑制位点，开展了一项关于细胞介导免疫的过继转移研究。通过输尿管结扎使13系豚鼠患尿毒症。分离淋巴结细胞并通过以下三种方式进行转移：第1组：结核菌素敏感的非尿毒症供体至非免疫的非尿毒症受体；第2组：结核菌素敏感的非尿毒症供体至非免疫的尿毒症受体；第3组：结核菌素敏感的尿毒症供体至非免疫的非尿毒症受体。第1组和第3组转移受体的皮肤试验反应没有差异，尽管第3组的尿毒症供体已失去其皮肤试验反应性。第2组中结核菌素敏感性的转移未成功。这些结果表明，尿毒症状态会抑制先前建立的皮肤试验反应性，但不会阻止致敏T淋巴细胞传递细胞免疫。
