Beatty D W, Dowdle E B
Clin Exp Immunol. 1979 Mar;35(3):433-42.
Blastogenic responses of normal human peripheral blood lymphocytes cultured in media supplemented with serum from children with kwashiorkor were, on average, 47.7% of those observed when the same cells were cultured in the presence of normal AB serum. Incorporation of radioactive uridine was also diminished in the presence of normal AB serum. Incorporation of radioactive uridine was also diminished in the presence of kwashiorkor serum indicating that lectin-induced RNA synthesis was also affected. The kwashiorkor serum effect was not due to a cytotoxic action nor could it be attributed to the presence of saccharides or other inhibitors of the inducing lectins. Mixing experiments showed that kwashiorkor serum was not inhibitory, but that it lacked factors present in normal serum that are required for optimal lymphocyte blastogenesis. The deficiency of these factors could largely be rectified by supplementing kwashiorkor serum with an ultrafiltrate of normal serum containing components with molecular weights of less than 500 Daltons. We conclude that nutritional deprivation of severity sufficient to cause kwashiorkor leads to a deficiency of low molecular weight lymphocyte growth factors. This lack may contribute to the immunodeficiency associated with the disease.
在添加了夸休可尔症患儿血清的培养基中培养的正常人外周血淋巴细胞的增殖反应,平均而言,仅为在正常AB血清存在下培养相同细胞时所观察到的增殖反应的47.7%。在正常AB血清存在的情况下,放射性尿苷的掺入也减少了。在夸休可尔症血清存在的情况下,放射性尿苷的掺入同样减少,这表明凝集素诱导的RNA合成也受到了影响。夸休可尔症血清的作用并非由于细胞毒性作用,也不能归因于糖类或诱导凝集素的其他抑制剂的存在。混合实验表明,夸休可尔症血清并无抑制作用,而是缺乏正常血清中存在的、淋巴细胞最佳增殖所必需的因子。通过用分子量小于500道尔顿的正常血清超滤物补充夸休可尔症血清,这些因子的缺乏在很大程度上可以得到纠正。我们得出结论,严重到足以导致夸休可尔症的营养缺乏会导致低分子量淋巴细胞生长因子的缺乏。这种缺乏可能导致与该疾病相关的免疫缺陷。