Epstein-Barr virus transformation of B lymphocytes from IgA nephropathy patients and first-degree relatives results in increased immunoglobulin synthesis not restricted to IgA.
Epstein-Barr virus transformation of B lymphocytes from IgA nephropathy patients and first-degree relatives results in increased immunoglobulin synthesis not restricted to IgA.
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来自 IgA 肾病患者和一级亲属的 B 淋巴细胞经 Epstein-Barr 病毒转化，导致免疫球蛋白合成增加，而不仅限于 IgA。
DOI：
10.1016/s0272-6386(12)80251-4
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Julian,BA
中科院分区：
文献类型：
--
作者：
Jackson,S;Galla,JH;Kirk,KA;Thorn,BT;Julian,BA
为了研究伊加肾病（IgAN）患者中不依赖于T细胞调节的B细胞活化模式，用EB病毒转化了67名IgAN患者、15名家族性疾病患者的一级亲属和13名正常对照的外周血单个核细胞。病毒（EBV）。测定这些转化细胞的培养上清液的IgG、伊加和IgM水平，并比较在三个群体上获得的结果。与正常对照组相比，IgA肾病患者以及一级亲属的EBV转化细胞分泌的所有三种同种型的水平显著升高。然而，在比较分泌的同种型的比率中，确定了与正常对照相比，这两个群体的细胞合成了相对于IgG和IgM更多的伊加。我们的研究结果表明：（1）易受EBV激活的B细胞群在IgAN患者中增加;（2）这种“可激活”的B淋巴细胞群是多克隆的，不限于伊加类;和（3）尽管IgAN中可能存在原发性B细胞异常，但在发病机制中可能存在额外的缺陷，因为临床上未受影响的亲属的细胞表现出与患者相似的模式。
In order to study B-cell activation patterns independent of T-cell regulation in patients with IgA nephropathy (IgAN), peripheral blood mononuclear cells from 67 patients with IgAN,15 first-degree relatives of patients with familial disease, and 13 normal controls were transformed with Epstein-Barr virus (EBV). Culture supernatants of these transformed cells were assayed for levels of IgG, IgA, and IgM, and results obtained on the three populations were compared. EBV-transformed cells of IgAN patients, as well as the population of first-degree relatives, secreted significantly elevated levels of all three isotypes as compared with the normal controls. However, in comparing ratios of secreted isotypes, it was determined that more IgA relative to IgG and IgM was synthesized by cells of these two populations as compared with the normal controls. Our results imply that (1) the population of B cells susceptible to EBV activation is increased in IgAN patients; (2) this population of “activatable” B lymphocytes is polyclonal and not restricted to the IgA class; and (3) even though there may be a primary B-cell abnormality in IgAN, an additional defect(s) is probably operative in the pathogenesis, since cells of clinically unaffected relatives behaved in a pattern similar to that of patients.