Salata M, Golbus J, Richardson B C
Department of Internal Medicine, University of Michigan, Ann Arbor.
Clin Exp Immunol. 1988 Mar;71(3):439-44.
Systemic lupus erythematosus is an autoimmune disease characterized by B-cell hyperactivity, resulting in polyclonal hypergammaglobulinaemia. One mechanism potentially resulting in excessive immunoglobulin synthesis is a diminished response to inhibitory signals. To test this hypothesis, anti-IgG antisera was used to inhibit pokeweed mitogen activation of cultured lymphocytes from lupus patients and controls. Inhibition of IgG secretion by B cells from lupus patients required more than 75 times as much anti-IgG as normal controls (P less than 0.005), indicating that lupus lymphocytes are hyporesponsive to this inhibitory signal. Similar studies with DR3+ controls demonstrated that diminished responsiveness to anti-IgG inhibition may in part be associated with the HLA-DR3 allele. Defects in this inhibitory mechanism may play a role in the B-cell hyperactivity observed in lupus.
系统性红斑狼疮是一种自身免疫性疾病，其特征为B细胞功能亢进，导致多克隆高丙种球蛋白血症。一种可能导致免疫球蛋白过度合成的机制是对抑制性信号的反应减弱。为验证这一假设，使用抗IgG抗血清抑制来自狼疮患者和对照的培养淋巴细胞的商陆有丝分裂原激活。狼疮患者B细胞的IgG分泌抑制所需的抗IgG量是正常对照的75倍以上（P<0.005），表明狼疮淋巴细胞对这种抑制性信号反应低下。对DR3+对照的类似研究表明，对抗IgG抑制反应减弱可能部分与HLA-DR3等位基因有关。这种抑制机制的缺陷可能在狼疮中观察到的B细胞功能亢进中起作用。
