Epstein-Barr virus-related antibody patterns in ataxia-telangiectasia.
Epstein-Barr virus-related antibody patterns in ataxia-telangiectasia.
复制标题
共济失调毛细血管扩张症中与 Epstein-Barr 病毒相关的抗体模式。
DOI：
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发表时间：
1979
影响因子：
4.6
通讯作者：
O. Sanal
中科院分区：
文献类型：
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作者：
Berkel Ai;W. Henle;G. Henle;George Klein;F. Ersoy;O. Sanal
研究人员测定了 27 名共济失调毛细血管扩张症 (AT) 患者及其 22 名健康家庭成员、22 名患有其他疾病的患者（其中 10 名患有白塞氏病和 10 名患有各种原发性免疫缺陷）、15 名健康家庭成员以及 23 名不相关的健康对照者的 Epstein-Barr 病毒相关抗体滴度。 AT患者的病毒衣壳抗原（VCA）高抗体滴度（大于或等于1:320）发生率增加（55.6%），EB病毒（EBV）诱导的早期抗原（EA）抗体发生率也较高（48.2%），但EBV相关核抗原（EBNA）抗体滴度较低（低于1:10）的病例占44.2%。与对照组相比，抗 VCA 的几何平均值高出三到四倍，抗 EBNA 的几何平均值低六倍。患有其他疾病的患者与对照组没有显着差异，只是抗EBNA滴度低于1:10的发生率较高（38.1% vs 4--5%）。根据总淋巴细胞和 E-玫瑰花结细胞计数以及皮试反应检测，抗 EBNA 滴度较低的 AT 患者往往比抗 EBNA 滴度中等的 AT 患者存在更严重的 T 细胞缺陷。结果支持这样的假设：需要功能正常的 T 细胞系统从携带 EBV 基因组的细胞中释放 EBNA，以实现抗 EBNA 的初始和持续产生。
Epstein-Barr virus-related antibody titres were determined in twenty-seven patients with ataxia-telangiectasia (AT) and twenty-two healthy members of their families, in twenty-two patients with other diseases, among them ten with Behçet's disease and ten with various primary immune deficiencies, and fifteen healthy members of their families, and in twenty-three unrelated healthy controls. The AT patients showed an increased incidence (55.6%) of high antibody titres (greater than or equal to 1:320) to viral capsid antigen (VCA), and also a high incidence (48.2%) of antibodies to Epstein-Barr virus (EBV) induced early antigens (EA), but low titres (less than 1:10) of antibodies to the EBV-associated nuclear antigen (EBNA) in 44.2% of the cases. The geometric means of anti-VCA were three-to four-fold higher, and of anti-EBNA six-fold lower, than those of the control groups. The patients with the other diseases did not differ significantly from the controls except for a higher incidence of anti-EBNA titres of less than 1:10 (38.1% vs 4--5%). AT patients with low anti-EBNA titres tended to have more advanced T cell deficiencies than AT patients with moderate anti-EBNA titres, as detected by counts of total lymphocytes and E-rosetting cells, and skin test responses. The results support the hypothesis that a functioning T cell system is required to release EBNA from EBV genome-carrying cells for initial and maintained production of anti-EBNA.