INTERLEUKIN 6 SERUM LEVELS IN SOLID ORGAN TRANSPLANT RECIPIENTS

实体器官移植受者发生淋巴组织增生 EB病毒（EBV）感染的B细胞的病症。 此外，本发明还提供了一种方法， 白细胞介素-6（IL-6）促进体外EBV感染的B细胞的生长， in vivo. 目的：研究IL-6在原发性肝癌发生发展中的作用。 移植后淋巴组织增生性疾病（PTLD），我们已经测量了 14例实体器官移植受者血清IL-6水平 其中6名未发生PTLD的患者IL-6水平正常 (5-15 U/ml）持续移植后45至215天。 相比之下，6/7 PTLD患者血清IL-6水平异常升高 （85 - 1040 U/ml）。 在所有 其中1例血清IL-6水平异常升高， 在诊断PTLD之前（3 - 45天）。 1例显微镜下PTLD患者 移植肾的血清IL-6水平相对正常（18 U/ml）。 最后，17天后死于败血症的14名患者中有1名 移植物在死亡前具有异常高的IL-6水平（50 - 103U/ml）。 5个单细胞悬液的培养上清液中的平均IL-6水平 PTLD病变大于1500 U/ml，而PTLD患者的平均IL-6水平大于1500 U/ml。 急性胰腺炎患者外周血培养上清 传染性单核细胞增多症均小于15 U/ml。 所有这些 研究结果表明，一般来说，IL-6水平异常升高， 提示IL-6可能在PTLD患者血清中起作用， PTLD的发病机制。

Recipients of solid organ transplants develop lymphoproliferative disorders of Epstein-Barr virus (EBV)-infected B cells. In addition, interleukin-6 (IL-6) promotes growth of EBV-infected B cells in vitro and in vivo. To study a potential role of IL-6 in the development of post-transplant lymphoproliferative disorders (PTLD), we have measured IL-6 levels in serum samples of 14 solid organ transplant recipients. Six of these patients who did not develop PTLD had normal IL-6 levels (5-15 U/ml) for 45 to 215 days post transplant. In contrast, 6 of 7 patients who developed PTLD had abnormally elevated serum IL-6 levels (85-1040 U/ml)at various timepoints post transplant (5-310 days). In all but one of these 7 cases, serum IL-6 levels were abnormally elevated before (3-45 days) PTLD was diagnosed. One patient with microscopic PTLD of the transplanted kidney had relatively normal serum IL-6 levels (18 U/ml). Finally, one of the 14 patients who died of sepsis 17 days post transplant had abnormally high IL-6 levels (50-103 U/ml) prior to death. Mean IL-6 levels in the culture supernatants of 5 single cell suspended PTLD lesions were greater than 1500 U/ml, while mean IL-6 levels in culture supernatants of peripheral blood of patients with acute infectious mononucleosis were less than 15 U/ml. Together, these findings demonstrate that, generally, IL-6 levels are abnormally elevated in sera of PTLD patients, and suggest that IL-6 may have a role in the pathogenesis of PTLD.