Tarcic N, Naor D
Eur J Immunol. 1982 Nov;12(11):961-6. doi: 10.1002/eji.1830121112.
Previous studies suggested that trinitrophenyl (TNP)-modified syngeneic red cells induced humoral autoimmune response in mice with defective T cell function but not in normal mice. The ability of modified self antigen to induce autoimmune response in immunodeficient mice was further explored using the delayed-type hypersensitivity (DTH) as an assay system. Mice were immunized with syngeneic TNP-modified spleen cells (TNP-SC) and challenged by syngeneic nonmodified concanavalin A (Con A) or lipopolysaccharide (LPS)-stimulated spleen cells injected into their footpads. The DTH response was assessed 24, 48 and 72 h later by measuring the footpad swelling and was transferred to naive recipients with enriched T cells from TNP-SC-immunized irradiated A mice but not with serum or non-T cells. Adult thymectomized, X-irradiated (250 rds) and cyclophosphamide-treated mice injected with syngeneic TNP-SC generated a DTH response when subsequently challenged with syngeneic lymphoblasts (induced with Con A or LPS) but not when challenged with allogeneic blast cells. In contrast, normal mice treated in a similar manner exhibited a much less significant DTH response. SC incubated 1 to 3 h with Con A failed to elicit the DTH response of immunodeficient mice previously injected with TNP-SC. Both lymphoblasts that were induced in vitro with Con A diluted in fetal calf serum or in normal mouse serum-containing media, and lymphoblasts that were induced in vivo by interleukin 2 elicited DTH responses in X-irradiated, TNP-SC immunized mice. The syngeneic DTH response of the immunodeficient mice injected with TNP-SC was abrogated when they were simultaneously transplanted with syngeneic SC or nylon wool-passed syngeneic SC. If the transplanted splenocytes had been treated with anti-Thy-1 antiserum and complement they failed to abrogate the syngeneic-DTH response of the above mentioned mice. This result suggests that suppressor cells are programmed to control the autoimmune response induced with modified self antigens.
先前的研究表明，三硝基苯基（TNP）修饰的同基因红细胞在T细胞功能缺陷的小鼠中可诱导体液自身免疫反应，但在正常小鼠中则不会。使用迟发型超敏反应（DTH）作为检测系统，进一步探究了修饰的自身抗原在免疫缺陷小鼠中诱导自身免疫反应的能力。用同基因TNP修饰的脾细胞（TNP-SC）免疫小鼠，然后将同基因未修饰的伴刀豆球蛋白A（Con A）或脂多糖（LPS）刺激的脾细胞注射到其足垫中进行激发。24、48和72小时后，通过测量足垫肿胀来评估DTH反应，并将其转移至用来自TNP-SC免疫的经照射的A小鼠的富集T细胞处理的未致敏受体，而不是用血清或非T细胞。成年胸腺切除、经X射线照射（250拉德）并用环磷酰胺处理的小鼠，注射同基因TNP-SC后，随后用同基因淋巴细胞（由Con A或LPS诱导）激发时会产生DTH反应，但用异基因胚细胞激发时则不会。相比之下，以类似方式处理的正常小鼠表现出的DTH反应要弱得多。用Con A孵育1至3小时的脾细胞未能引发先前注射TNP-SC的免疫缺陷小鼠的DTH反应。在含有胎牛血清或含正常小鼠血清的培养基中用Con A体外诱导的淋巴细胞，以及在体内由白细胞介素2诱导的淋巴细胞，均可在经X射线照射、TNP-SC免疫的小鼠中引发DTH反应。注射TNP-SC的免疫缺陷小鼠同时移植同基因脾细胞或经尼龙毛处理的同基因脾细胞时，其同基因DTH反应被消除。如果移植的脾细胞用抗Thy-1抗血清和补体处理，则它们无法消除上述小鼠的同基因DTH反应。这一结果表明，抑制细胞被编程以控制由修饰的自身抗原诱导的自身免疫反应。
