Cornelius E A
Am J Pathol. 1978 Mar;90(3):675-88.
Perinatal C57BL/1 mice given injections of (SJL/J X C57BL/1)F1 spleen cells developed a highly lethal runting syndrome, designated host-versus-graft disease (HVGD). The mortality was related to the dosage of F1 cells. Acute pathologic changes resembled those occurring in parent leads to F1 graft-versus-host disease (GVHD), except for more pronounced plasmacytosis. Mice suffering from HVGD recovered clinically with no sequelae except for a slight increase in the incidence of lymphomas over control mice. Such mice were hyperreactive to F1 cells utilized to initiate the original HVGD syndrome. Most of the tumors developed in those animals receiving the initial injection of F1 spleen cells within 24 hours of birth. Tumor incidence was unrelated to the clinical severity of HVGD. By contrast, GVHD in the same strain combination resulted in a much higher incidence of lymphomas in a much shorter time. Parental strain cells were detectable in the F1 hosts up to the time of tumor development. HVGD has a low tumor induction potential; GVHD has a high tumor induction potential.
给围产期的C57BL/1小鼠注射(SJL/J×C57BL/1)F1脾细胞后,会引发一种高度致命的发育不良综合征,称为宿主抗移植物病(HVGD)。死亡率与F1细胞的剂量有关。急性病理变化类似于亲本导致F1移植物抗宿主病(GVHD)时发生的变化,只是浆细胞增多更为明显。患有HVGD的小鼠临床康复,除了淋巴瘤发病率比对照小鼠略有增加外,无后遗症。此类小鼠对用于引发原始HVGD综合征的F1细胞反应过度。大多数肿瘤发生在出生后24小时内接受初始F1脾细胞注射的那些动物身上。肿瘤发生率与HVGD的临床严重程度无关。相比之下,相同品系组合中的GVHD在更短时间内导致更高的淋巴瘤发病率。直到肿瘤发生时,在F1宿主中都能检测到亲本品系细胞。HVGD的肿瘤诱导潜力低;GVHD的肿瘤诱导潜力高。