Transfer of resistance to Schistosoma mansoni in Biomphalaria glabrata by allografts of amoebocyte-producing organ.
Transfer of resistance to Schistosoma mansoni in Biomphalaria glabrata by allografts of amoebocyte-producing organ.
复制标题
通过变形虫细胞产生器官的同种异体移植物转移对光滑双脐虫的曼氏血吸虫抗性。
作者：
J. Sullivan;J. Spence
将变形细胞生成器官 (APO) 的同种异体移植物异位移植到来自 13-16-R1（抗血吸虫种）或 NIH 白化种供体的血吸虫敏感 NIH 白化种光滑 Biomphalaria 光滑种种中。在植入后 (PI) 第 3、7-8、14-15、21、28-33 或 47-71 天，同种异体移植受者分别接触 50 个曼氏血吸虫毛蚴，随后监测孢子囊和尾蚴的发育。相对于未受感染的蜗牛和 NIH 白化 APO 的接受者，从 PI 7 天到实验结束，13-16-R1 APO 的接受者的感染率明显较低。这种明显的耐药性转移的机制尚不清楚，但假设它可能涉及嵌合，即通过植入 13-16-R1 APO 产生具有耐药表型的血细胞，或通过植入可诱导受体血细胞产生细胞毒性的可溶性“耐药因子”进行合成，或两者兼而有之。
Allografts of amoebocyte-producing organ (APO) were implanted heterotopically into the schistosome-susceptible NIH albino stock of Biomphalaria glabrata from either 13-16-R1 (a schistosome-resistant stock) or NIH albino donors. At 3, 7-8, 14-15, 21, 28-33, or 47-71 days postimplantation (PI), allograft recipients were exposed to 50 miracidia each of Schistosoma mansoni and subsequently monitored for development of sporocysts and cercariae. Relative to untampered snails and recipients of NIH albino APOs, recipients of 13-16-R1 APOs showed significantly lower infection rates from 7 days PI until the end of the experiment. The mechanism for this apparent transfer of resistance is unknown, but hypothetically it may involve chimerism, i.e., production of hemocytes with the resistant phenotype by implanted 13-16-R1 APOs, or synthesis by the implant of soluble "resistance factors" that induce cytotoxicity in recipient hemocytes, or both.