INTERLEUKIN 6 SERUM LEVELS IN SOLID ORGAN TRANSPLANT RECIPIENTS

实体器官移植的受者出现淋巴增生性疾病 EB病毒(EBV)感染的B细胞疾病此外, 白介素6促进EB病毒感染B细胞的体外生长和 在活体内。研究IL-6在血管内皮细胞瘤发生发展中的作用 移植后淋巴增生性疾病(PTLD)，我们测量了 14例实体器官移植受者血清IL-6水平 其中6名未发展为PTLD的患者IL-6水平正常 (5~15U/ml)，移植后45~215天。相比之下，7次中的6次 PTLD患者血清IL-6水平异常升高 (85~1040U/ml)，移植后不同时间(5~310天)。总而言之， 但在这7例中，有一例血清IL-6水平异常升高 在诊断为PTLD之前(3-45天)。显微镜下PTLD患者1例 移植肾患者的血清IL-6水平相对正常(18 U/ml)。最后，17天后死于脓毒症的14名患者中的一名 移植患者死前IL-6水平异常高(50-103U/ml)。 5种单细胞悬液培养上清液中IL-6的平均水平 PTLD病变大于1500U/ml，而患者的平均IL-6水平 急性白血病患者外周血培养上清液的检测 传染性单核细胞增多症低于15U/ml。加起来，这些 研究结果表明，一般说来，IL-6水平异常升高 提示IL-6可能在PTLD的发病机制中起一定作用。 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.