Kaneko H, Kondo N, Motoyoshi F, Mori S, Kobayashi Y, Ozawa T, Orii T
Department of Pediatrics, Gifu University School of Medicine, Japan.
Scand J Immunol. 1990 Nov;32(5):483-9. doi: 10.1111/j.1365-3083.1990.tb03188.x.
Five heterogeneous IgA-immunodeficient patients were analysed for expression of the alpha-chain gene. The number of surface IgA-bearing B cells was low in four patients. Southern blot analysis indicated no deletion of immunoglobulin structural genes coding for C alpha or alpha switching-region genes. The number of surface IgM and IgA double-bearing B cells increased in some patients. Addition of recombinant interleukin 4 (rIL-4), rIL-5, and rIL-6 to the normal B cells enhanced IgA production. However, B cells of the patients showed no or one-third lower IgA production in response to these lymphokines, even though there was proliferation. rIL-4, rIL-5, and rIL-6 induced low or no expression of alpha mRNA of the patients' B cells. These results suggested that the patients lacked B cells able to produce transcripts for the IgA heavy chain, and that some patients' B cells might be defective at the switch-recombination process from mu to alpha or from mu and alpha to alpha.
对五名异质性IgA免疫缺陷患者进行了α链基因表达分析。四名患者中表达表面IgA的B细胞数量较低。Southern印迹分析表明,编码Cα的免疫球蛋白结构基因或α转换区基因未发生缺失。部分患者中表达表面IgM和IgA的双阳性B细胞数量增加。向正常B细胞中添加重组白细胞介素4(rIL-4)、rIL-5和rIL-6可增强IgA的产生。然而,尽管患者的B细胞发生了增殖,但对这些细胞因子的反应中,其IgA产生未增加或仅增加了三分之一。rIL-4、rIL-5和rIL-6诱导患者B细胞的α mRNA低表达或不表达。这些结果表明,这些患者缺乏能够产生IgA重链转录本的B细胞,并且部分患者的B细胞在从μ到α或从μ和α到α的转换重组过程中可能存在缺陷。