Allotype Analysis to Distinguish the Origin of Varicella-Zoster Virus Immunoglobulin G After Allogeneic Stem Cell Transplantation.
Allotype Analysis to Distinguish the Origin of Varicella-Zoster Virus Immunoglobulin G After Allogeneic Stem Cell Transplantation.
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同种异型分析以区分同种异体干细胞移植后水痘带状疱疹病毒免疫球蛋白 G 的起源。
DOI：
10.1016/j.bbmt.2013.04.007
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
et al.
中科院分区：
文献类型：
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作者：
Yamazaki R;Nakasone H;Kanda Y;et al.
水痘带状疱疹病毒（VZV）再激活是异基因造血干细胞移植（HSCT）后常见的并发症。尽管之前的研究表明细胞免疫对于抑制病毒再激活很重要，但体液免疫对水痘带状疱疹病毒的作用评价甚少。我们分析了 50 个 HSCT 受者-供者对的免疫球蛋白 G (IgG) 重链恒定区的遗传多态性，以区分供者衍生的抗体和受体衍生的抗体。十二对提供了有关 IgG 起源的信息，因为供体 (n = 3) 或受者 (n = 9) 的 IgG1m(f) 同种异型纯合无效。在这 9 名纯合子无效受体中，通过酶联免疫吸附测定法测量了针对 VZV 的同种异型特异性 IgG，并与麻疹 IgG 进行了比较。所有 9 名纯合子无效受体在 HSCT 后均接受了超过 1 年的监测，其中有（n = 4，局部带状疱疹）或没有（n = 5）临床 VZV 疾病。在 3 名 VZV 疾病患者中，在 VZV 疾病发作后 HSCT 后 500 至 700 天期间，供体来源的抗 VZV IgG 升高。 1 名在 HSCT 前患有 VZV 疾病的患者，供体来源的 VZV IgG 在 HSCT 后 3 个月内升高。另一方面，2 名接受 IgG1m(f) 无效供体的低强度调节 (RIC) 移植的患者，受者来源的抗 VZV IgG 维持超过 1 年，而 1 名接受常规调节的受者，其抗 VZV IgG 在 3 个月内下降。总之，受体浆细胞在 RIC 后仍能持续产生抗 VZV IgG。在没有症状的 VZV 重新激活的患者中，供体来源的抗 VZV IgG 的滴度未达到与健康病毒携带者中测量的滴度相当的水平。
Varicella-zoster virus (VZV) reactivation is a frequent complication after allogeneic hematopoietic stem cell transplantation (HSCT). Although previous studies have revealed that cellular immunity is important for suppressing reactivation, the role of humoral immunity against VZV has been poorly evaluated. We analyzed inherited polymorphisms in the immunoglobulin G (IgG) heavy chain constant regions of 50 HSCT recipient-donor pairs to distinguish donor-derived and recipient-derived antibodies. Twelve pairs were informative regarding the origin of IgG, since either the donors (n = 3) or recipients (n = 9) were homozygous null for the IgG1m(f) allotype. In these 9 homozygous-null recipients, allotype-specific IgG against VZV were measured by enzyme-linked immunosorbent assay and compared with measles-IgG. All 9 homozygous-null recipients were monitored for more than 1 year after HSCT, with (n = 4, localized zoster) or without (n = 5) clinical VZV disease. In 3 patients with VZV disease, donor-derived IgG against VZV was elevated between 500 to 700 days after HSCT after the episode of VZV disease. In 1 patient who suffered from VZV disease just before HSCT, donor-derived VZV IgG was elevated within 3 months after HSCT. On the other hand, 2 patients who received reduced-intensity conditioning (RIC) transplantation from an IgG1m(f) null donor maintained recipient-derived IgG against VZV for more than 1 year, whereas it was decreased within 3 months in 1 recipient who received conventional conditioning. In conclusion, the production of anti-VZV IgG by recipient plasma cells persists long after RIC. In patients without symptomatic VZV reactivation, donor-derived anti-VZV IgG did not reach titers comparable to those measured in healthy virus carriers.