Advani S H, D'Silva H, Gothoskar B P, Dinshaw K A, Nair C N, Gopalkrishna R, Talwalkar G V, Desai P B
Cancer. 1979 Feb;43(2):492-9. doi: 10.1002/1097-0142(197902)43:2<492::aid-cncr2820430214>3.0.co;2-l.
Defective cell-mediated immunity (CMI) occurs early in the course of Hodgkin's disease (HD) and may persist even two years after successful treatment. This has been confirmed by in vivo and in vitro tests performed on 51 untreated and 52 treated patients of HD. The grading of skin reponse in vivo to dinitrochlorobenzene (DNCB) correlated very well with the in vitro leukocyte migration inhibition (LMI) response against phytohemagglutinin (PHA). An inhibitory influence of HD patients' sera was demonstrated by LMI tests in vitro. The response of peripheral leukocytes from HD patients in the LMI tests could be augmented in vitro by addition of levamisole (an immuno-potentiator) to the culture medium, thus pointing to an intrinsic defect in Lymphocytes. The data indicate that defect at multiple sites in the immune system is responsible for persistent anergy in HD.
细胞介导免疫(CMI)缺陷在霍奇金病(HD)病程早期就已出现,甚至在成功治疗两年后仍可能持续存在。这已通过对51例未经治疗和52例已治疗的HD患者进行的体内和体外试验得到证实。体内对二硝基氯苯(DNCB)的皮肤反应分级与体外针对植物血凝素(PHA)的白细胞迁移抑制(LMI)反应密切相关。体外LMI试验证明了HD患者血清的抑制作用。在LMI试验中,通过向培养基中添加左旋咪唑(一种免疫增强剂),可在体外增强HD患者外周血白细胞的反应,从而表明淋巴细胞存在内在缺陷。数据表明,免疫系统多个部位的缺陷是HD持续无反应性的原因。