Cerny J, Essex M, Rich M A, Hardy W D
Int J Cancer. 1975 Feb 15;15(2):351-65. doi: 10.1002/ijc.2910150219.
Spontaneous regression and/or remission of Friend virus (FV)-induced splenic erythroblastic leukemia was observed in CD-1 mice infected with several isolates of FV. Regression of splenic tumor was accompanied by the loss of both specific FV-induced cell membrane antigen (FVMA) and virus group-specific antigens (gsa) from the spleen cells. The frequency (percentage) of immunoglobulin-positive cells (B) and thetapositive cells (T) in the spleen was markedly decreased during leukemia progression, but there was a subsequent increase during regression. The appearance of gsa-positive (gsa+) cells in peripheral blood correlated well with the early progressive and regressive phase of leukemia (up to 7 weeks after infection). Later, the presence of these cells became unpredictable in regard to status of disease. Gsa+ blood cells reappeared in most mice with regressed splenic tumors, suggesting persistence of the virus complex in the animals. Antibody responsiveness as determined by the numbers of hemolytic plaque-forming cells, PFC, after a single immunization with sheep red blood cells (SRBC), was suppressed in leukemia progression and recovered, spontaneously, during regression of leukemia. However, hemolytic PFC elicited by antigen in both progressors and regressors expressed the specific virus-induced membrane antigen, FVMA, detectable by the PFC-inhibition test with specific antiserum and complement. Recovery of immunological responsiveness also included the spontaneous appearance of virus-neutralizing antibody to FV. However, this was not paralleled by the appearance of antibody to FVMA. Traces of anti-FVMA antibody activity were occasionally detectable in serum of both progressors and regressors and did not correlate with virus neutralization, in individual mice; This may explain the susceptibility of regressors to secondary relapse and to reinfection.
在感染了几种弗氏病毒(FV)分离株的CD-1小鼠中,观察到FV诱导的脾红细胞性白血病的自发消退和/或缓解。脾肿瘤的消退伴随着脾细胞中特异性FV诱导的细胞膜抗原(FVMA)和病毒群特异性抗原(gsa)的丧失。在白血病进展过程中,脾中免疫球蛋白阳性细胞(B)和θ阳性细胞(T)的频率(百分比)显著降低,但在消退过程中随后增加。外周血中gsa阳性(gsa+)细胞的出现与白血病的早期进展和消退阶段密切相关(感染后长达7周)。后来,这些细胞的存在与疾病状态变得不可预测。gsa+血细胞在大多数脾肿瘤消退的小鼠中重新出现,表明病毒复合物在动物体内持续存在。通过用绵羊红细胞(SRBC)单次免疫后溶血空斑形成细胞(PFC)的数量测定的抗体反应性,在白血病进展过程中受到抑制,并在白血病消退期间自发恢复。然而,在进展期和消退期由抗原引发的溶血PFC均表达特异性病毒诱导的膜抗原FVMA,可通过用特异性抗血清和补体的PFC抑制试验检测到。免疫反应性的恢复还包括FV病毒中和抗体的自发出现。然而,这与FVMA抗体的出现并不平行。在进展期和消退期小鼠的血清中偶尔可检测到微量的抗FVMA抗体活性,且在个体小鼠中与病毒中和无关;这可能解释了消退期小鼠对二次复发和再感染的易感性。