Whittingham S, Pitt D B, Sharma D L, Mackay I R
Lancet. 1977 Jan 22;1(8004):163-6. doi: 10.1016/s0140-6736(77)91763-9.
A comparison of immune competence in 26 patients with Down syndrome in an institution and 26 matched healthy controls revealed an atypical pattern of T-cell immunodeficiency in the Down-syndrome patients. The patients with Down syndrome had a lymphocytosis in blood with high counts of T (and B) cells, but with impaired effector function of T cells as judged by anergy to dinitrochlorobenzene, low responsiveness to ubiquitous antigens which elicit delayed-type hypersensitivity reactions, and low mitogenic activity of non-stimulated and phytohaemagglutinin-stimulated lymphocytes in culture. Helper-T-cell function measured by the humoral immune response to flagellin was intact, and there were minor abnormalities of the B-cell system. Attempted restoration of T-cell function with levamisole was unsuccessful. This pattern of T-lymphocytosis with impaired effector function could be explained by "stress-deficiency" of the immune system consequent upon a heavy load of infection in early life.
对一所机构中26名唐氏综合征患者和26名匹配的健康对照者的免疫能力进行比较后发现,唐氏综合征患者存在非典型的T细胞免疫缺陷模式。唐氏综合征患者血液中淋巴细胞增多,T(和B)细胞计数较高,但T细胞的效应功能受损,这可通过对二硝基氯苯无反应、对引发迟发型超敏反应的普遍存在抗原反应性低以及培养中未刺激和植物血凝素刺激的淋巴细胞有丝分裂活性低来判断。通过对鞭毛蛋白的体液免疫反应测量的辅助性T细胞功能正常,B细胞系统有轻微异常。用左旋咪唑试图恢复T细胞功能未成功。这种效应功能受损的T淋巴细胞增多模式可以用生命早期感染负担过重导致的免疫系统“应激性缺陷”来解释。