Coutinho S G, Louis J A, Mauel J, Engers H D
Parasite Immunol. 1984 Mar;6(2):157-69. doi: 10.1111/j.1365-3024.1984.tb00789.x.
The following cell populations derived from lymph nodes of mice primed in vivo with living Leishmania major promastigotes were tested for their capacity to induce parasiticidal activity in L. major-infected macrophages: a L. major-primed lymph node cells, draining lymph node cells from mice primed by a subcutaneous injection of living L. major in Freund's Complete Adjuvant; b L. major-specific T blasts, i.e. blast T cells resulting from in vitro challenge of primed lymph node cells with L. major, c propagated L. major specific T blasts, i.e. blast T cells after propagation in vitro in antigen-free medium containing interleukin-2. Results indicate that cocultivation of these L. major specific lymphocyte populations with infected peritoneal exudate macrophages induced progressive destruction of intracellular L. major. This effect was antigen specific since similar populations obtained from mice primed either with ovalbumin or bovine serum albumin did not induce significant parasite killing. The various lymphocyte populations examined did not express cytolytic activity for syngeneic macrophages infected with L. major when tested in a short-term 51Cr release assay. These negative results could not be attributed to an inability of infected macrophages to be lysed by cytolytic lymphocytes since cytolytic T lymphocytes directed to H-2 alloantigens present on macrophages were perfectly capable of lysing these infected macrophages as revealed in a 4 h 51Cr release assay. Interestingly, infected macrophages from either BALB/c (H-2d), NZB (H-2d) or CBA (H-2k) mice were lysed by cytolytic T lymphocytes specific for their respective H-2 alloantigens as well as uninfected macrophages. These results suggest that H-2 expression on the surface of infected macrophages from either L. major susceptible or resistant mouse strains is sufficient to be detected by allogeneic cytolytic T lymphocytes.
对以下从小鼠体内用活的硕大利什曼原虫前鞭毛体致敏的淋巴结中获得的细胞群体,检测它们在感染硕大利什曼原虫的巨噬细胞中诱导杀寄生虫活性的能力:a 经硕大利什曼原虫致敏的淋巴结细胞,来自于在弗氏完全佐剂中皮下注射活的硕大利什曼原虫致敏的小鼠的引流淋巴结细胞;b 硕大利什曼原虫特异性T母细胞,即经体外将致敏的淋巴结细胞用硕大利什曼原虫攻击后产生的母细胞T细胞;c 传代的硕大利什曼原虫特异性T母细胞,即在含有白细胞介素-2的无抗原培养基中体外传代后的母细胞T细胞。结果表明,这些硕大利什曼原虫特异性淋巴细胞群体与感染的腹腔渗出巨噬细胞共培养可诱导细胞内硕大利什曼原虫的逐步破坏。这种效应是抗原特异性的,因为从用卵清蛋白或牛血清白蛋白致敏的小鼠获得的类似群体不会诱导显著的寄生虫杀伤。在短期51Cr释放试验中检测时,所检查的各种淋巴细胞群体对感染硕大利什曼原虫的同基因巨噬细胞不表现出细胞溶解活性。这些阴性结果不能归因于感染的巨噬细胞不能被细胞溶解淋巴细胞裂解,因为在4小时51Cr释放试验中显示,针对巨噬细胞上存在的H-2同种异体抗原的细胞溶解T淋巴细胞完全能够裂解这些感染的巨噬细胞。有趣的是,来自BALB/c(H-2d)小鼠、NZB(H-2d)小鼠或CBA(H-2k)小鼠的感染巨噬细胞被针对其各自H-2同种异体抗原的细胞溶解T淋巴细胞以及未感染的巨噬细胞裂解。这些结果表明,来自硕大利什曼原虫易感或抗性小鼠品系的感染巨噬细胞表面的H-2表达足以被同种异体细胞溶解T淋巴细胞检测到。