Inoue T, Okubo H, Kudo J, Ikuta T, Hachimine K, Shibata R, Yoshinari O, Fukada K, Yanase T
J Clin Immunol. 1984 May;4(3):235-41. doi: 10.1007/BF00914971.
The cellular basis of the pathogenesis of selective IgA deficiency (SIgAD) was investigated by examining surface immunoglobulin (SmIg) and in vitro pokeweed mitogen (PWM)-stimulated immunoglobulin (Ig) synthesis and by assaying in combination the counterpart lymphocytes from individuals with SIgAD and healthy donors. Peripheral blood lymphocytes (PBL) from 14 individuals with SIgAD synthesized normal amounts of IgG and IgM but did not synthesize normal amounts of IgA. Functional defects of lymphocytes for IgA synthesis were classified into four types: (i) B-lymphocyte dysfunction, (ii) increased function of suppressor T lymphocytes (Ts), (iii) decreased function of helper T lymphocytes (Th), and (iv) B-lymphocyte dysfunction and increased Ts function. The cells bearing SmIgG, SmIgM, and SmIgD were demonstrated at normal percentage ratios in all cases by immunofluorescent staining. The cells bearing SmIgA were at normal percentage ratios in the cases of T-lymphocyte dysfunction, while in the cases of B-lymphocyte defect SmIgA-bearing cells were reduced.
通过检测表面免疫球蛋白（SmIg）和体外商陆有丝分裂原（PWM）刺激的免疫球蛋白（Ig）合成，并联合检测选择性IgA缺乏症（SIgAD）患者和健康供体的相应淋巴细胞，研究了SIgAD发病机制的细胞基础。14例SIgAD患者的外周血淋巴细胞（PBL）合成正常量的IgG和IgM，但不合成正常量的IgA。淋巴细胞IgA合成的功能缺陷分为四种类型：（i）B淋巴细胞功能障碍，（ii）抑制性T淋巴细胞（Ts）功能增强，（iii）辅助性T淋巴细胞（Th）功能降低，以及（iv）B淋巴细胞功能障碍和Ts功能增强。通过免疫荧光染色，在所有病例中均显示携带SmIgG、SmIgM和SmIgD的细胞比例正常。在T淋巴细胞功能障碍的病例中，携带SmIgA的细胞比例正常，而在B淋巴细胞缺陷的病例中，携带SmIgA的细胞减少。
