Skibin A, Yeremiyahu T, Keynan A, Quastel M R
Clin Exp Immunol. 1980 Feb;39(2):386-94.
Immunological studies were carried out on two female patients with angioimmunoblastic lymphadenopathy (AIL). Both presented with fever, lymphadenopathy, hepatosplenomegaly, rash and apparent ampicillin hypersensitivity. During the active phase of the disease, cellular immunity was depressed and T cell blastogenesis induced by lectins was abnormal. In the first patient, a non-dialysable plasma factor was found that inhibited normal lymphocyte blastogenesis, the removal of which enhanced the activation of AIL lymphocytes. This inhibitory plasma factor was also observed in the second patient during relapse of the disease. The latter patient responded well to steroid and levamisole therapy, showing clinical remission and a return of in vivo and in vitro parameters of cellular immunity. Defective B cell regulation due to impaired suppressor function, followed by immunoglobulin overproduction, is suggested to occur in AIL.
对两名患有血管免疫母细胞性淋巴结病(AIL)的女性患者进行了免疫学研究。两人均表现出发热、淋巴结病、肝脾肿大、皮疹以及明显的氨苄青霉素超敏反应。在疾病的活动期,细胞免疫受到抑制,凝集素诱导的T细胞增殖异常。在第一名患者中,发现了一种不可透析的血浆因子,它抑制正常淋巴细胞增殖,去除该因子可增强AIL淋巴细胞的活化。在第二名患者疾病复发期间也观察到了这种抑制性血浆因子。后一名患者对类固醇和左旋咪唑治疗反应良好,表现出临床缓解以及细胞免疫的体内和体外参数恢复正常。提示AIL中发生由于抑制功能受损导致的B细胞调节缺陷,继而出现免疫球蛋白过度产生。