Crawford D H, Edwards J M, Sweny P, Hoffbrand A V, Janossy G
Int J Cancer. 1981 Dec;28(6):705-9. doi: 10.1002/ijc.2910280608.
Peripheral blood lymphocytes from normal seropositive donors and renal transplant recipients on various immunosuppressive regimens have been tested for their ability to mount a cytotoxic response when cultured with autologous EB virus-infected B cells and thereby to cause regression of proliferating b-cell foci. Cultures from 10 normal seropositive donors all showed the normal pattern of regression. Lymphocytes from patients receiving Cyclosporin A therapy with or without prednisolone completely failed to cause regression, thus allowing B-cell lines to proliferate unchecked. Cells from two of 17 patients treated with azathioprine and prednisone also failed to cause regression. The cells from the remaining 15 individuals showed regression response varying from minimal to normal. These results suggest a mechanism by which EB virus-related tumours may arise in immunosuppressed renal allograft recipients.
对来自正常血清反应阳性供体以及接受各种免疫抑制方案治疗的肾移植受者的外周血淋巴细胞进行了检测，检测其与自体感染EB病毒的B细胞共同培养时产生细胞毒性反应的能力，进而导致增殖性B细胞灶消退的能力。来自10名正常血清反应阳性供体的培养物均显示出正常的消退模式。接受环孢素A治疗（无论是否联用泼尼松龙）的患者的淋巴细胞完全无法导致消退，从而使B细胞系不受抑制地增殖。17名接受硫唑嘌呤和泼尼松治疗的患者中有两名患者的细胞也无法导致消退。其余15名个体的细胞显示出从轻微到正常的消退反应。这些结果提示了一种机制，通过该机制，EB病毒相关肿瘤可能在免疫抑制的肾移植受者中发生。
