Cooperband S R, Rosen F S, Kibrick S
J Clin Invest. 1968 Apr;47(4):836-47. doi: 10.1172/JCI105777.
Circulating lymphocytes from patients with congenital X-linked agammaglobulinemia, sporadic congenital agammaglobulinemia, and acquired agammaglobulinemia have been cultured in vitro. They have been shown to proliferate in a normal manner under stimulus of phytohemagglutinin and antigens to which the patient was sensitized. Agammaglobulinemic cells have been shown to synthesize protein at a rate similar to that of normal cells, and the character of the extracellular protein produced is also similar. Agammaglobulinemic lymphocytes have been found to produce a small quantity of immunoglobulin G, similar to that found in normal cell cultures. The quantity of immunoglobulin produced may be increased by exposure of the cells to phytohemagglutinin. From these data, it appears that the basic lesion responsible for agammaglobulinemia is not a deficiency in lymphocyte-mediated antigen recognition or cellular proliferation. It would also appear that the basic deficiency in these disorders does not involve the structural or regulatory genes necessary for the synthesis of immunoglobulins. By exclusion, the pathogenesis of the deficiency would appear to involve cells other than circulating lymphocytes.
对患有先天性X连锁无丙种球蛋白血症、散发性先天性无丙种球蛋白血症和获得性无丙种球蛋白血症患者的循环淋巴细胞进行了体外培养。结果显示,在植物血凝素和患者致敏抗原的刺激下,这些淋巴细胞能以正常方式增殖。已证明无丙种球蛋白血症细胞合成蛋白质的速率与正常细胞相似,且所产生的细胞外蛋白质的特性也相似。已发现无丙种球蛋白血症淋巴细胞能产生少量免疫球蛋白G,这与正常细胞培养中发现的情况类似。通过使细胞接触植物血凝素,所产生的免疫球蛋白量可能会增加。从这些数据来看,导致无丙种球蛋白血症的基本病变似乎并非淋巴细胞介导的抗原识别或细胞增殖缺陷。这些疾病的基本缺陷似乎也不涉及免疫球蛋白合成所需的结构或调节基因。通过排除法,这种缺陷的发病机制似乎涉及循环淋巴细胞以外的细胞。