Björkholm M, Holm G, De Faire U, Mellsted H
Scand J Haematol. 1977 Oct;19(4):396-404. doi: 10.1111/j.1600-0609.1977.tb01491.x.
We studied the immunocompetence of 6 healthy twins, whose monozygotic or dizygotic same-sexed twin partner had died from Hodgkin's disease. Lymphocyte DNA synthesis induced by concanavalin A was markedly reduced at 3 different concentrations in all twins compared to an age-matched group of healthy controls. The lymphocyte response to pokeweed mitogen and to phytohaemagglutinin was also impaired. PPD induced lymphocyte DNA synthesis was low in 3 twins and correlated well with their delayed skin hypersensitivity to the antigen. One twin was completely anergic to 3 different skin antigens. The mean total blood lymphocyte count did not differ from that of controls. There was no change in T or B-lymphocyte subpopulations. The presence of a functional lymphocyte deficiency in all twins strongly suggests that the immunodeficiency in Hodgkin's disease is partly caused by genetic and/or environmental factors.
我们研究了6对健康双胞胎的免疫能力,他们的同卵或异卵同性双胞胎伴侣死于霍奇金病。与年龄匹配的健康对照组相比,在所有双胞胎中,3种不同浓度的伴刀豆球蛋白A诱导的淋巴细胞DNA合成均显著降低。对商陆有丝分裂原和植物血凝素的淋巴细胞反应也受损。3名双胞胎中PPD诱导的淋巴细胞DNA合成较低,且与他们对抗原的迟发性皮肤超敏反应密切相关。一名双胞胎对3种不同的皮肤抗原完全无反应。总血淋巴细胞计数的平均值与对照组无差异。T或B淋巴细胞亚群没有变化。所有双胞胎中存在功能性淋巴细胞缺陷,这有力地表明霍奇金病中的免疫缺陷部分是由遗传和/或环境因素引起的。