Mackaness G B, Hill W C
J Exp Med. 1969 May 1;129(5):993-1012. doi: 10.1084/jem.129.5.993.
The specificity of anti-lymphocyte globulin (ALG) has been used to analyze an immune mechanism which is mediated by immunologically committed lymphoid cells to the apparent exclusion of humoral antibody. Rabbit antimouse lymphocyte globulin completely suppressed the immunity which can be passively transferred with Listeria-immune lymphoid cells from actively infected donors. When prospective donors were given a single dose of 1.0 mg of ALG, it remained active against immune lymphoid cells transferred 24 hr later; yet immune cells in the spleens of donors could not be inactivated in situ by even larger doses of ALG given 24 hr prior to cell harvest. In keeping with this finding, the immunity to reinfection with Listeria was not suppressed by a single dose of ALG, indicating that the immunologically active cells in the spleen are not accessible to intravenously administered ALG. On the other hand, protracted treatment with ALG did abolish most of the memory of a previous infection in intact animals. From this and other evidence, it was concluded that immunologically committed cells are vulnerable to attack by ALG only if they circulate. While in circulation, they make contact both with ALG and the phagocytic elements of the reticuloendothelial system which appear to be responsible for their destruction. Four lines of evidence indicated that the suppression of anti-Listeria resistance with ALG depends upon destruction of immune lymphoid cells and not to any action it has on host macrophages. It is possible to infer from this that immunity to L. monocytogenes depends upon a two cell system in which the donor lymphoid cells provide the immunological reactivity to the organism and recipient macrophages provide the mechanism through which resistance is expressed. Accompanying papers provide additional support for this view, and reasons for believing that delayed-type hypersensitivity and acquired cellular resistance are mediated by the same population of immunologically committed lymphoid cells.
抗淋巴细胞球蛋白（ALG）的特异性已被用于分析一种免疫机制，该机制由免疫致敏淋巴细胞介导，明显排除了体液抗体的作用。兔抗小鼠淋巴细胞球蛋白完全抑制了可通过来自主动感染供体的李斯特菌免疫淋巴细胞被动转移的免疫力。当预期供体给予单剂量1.0mg的ALG时，它对24小时后转移的免疫淋巴细胞仍有活性；然而，即使在细胞收获前24小时给予更大剂量的ALG，供体脾脏中的免疫细胞也不能在原位被灭活。与这一发现一致的是，单剂量的ALG并不能抑制对李斯特菌再感染的免疫力，这表明静脉注射的ALG无法作用于脾脏中的免疫活性细胞。另一方面，长期使用ALG确实消除了完整动物先前感染的大部分记忆。基于这一发现及其他证据得出结论，免疫致敏细胞只有在循环时才易受ALG攻击。在循环过程中，它们与ALG以及网状内皮系统的吞噬成分接触，而后者似乎负责其破坏。四条证据表明，用ALG抑制抗李斯特菌抵抗力取决于免疫淋巴细胞的破坏，而非其对宿主巨噬细胞的任何作用。由此可以推断，对单核细胞增生李斯特菌的免疫力依赖于一个双细胞系统，其中供体淋巴细胞提供对该生物体的免疫反应性，受体巨噬细胞提供表达抵抗力的机制。相关论文为这一观点提供了额外支持，以及认为迟发型超敏反应和获得性细胞抵抗力由同一群免疫致敏淋巴细胞介导的理由。
