Recipient’s immune responses are an important factor in allograft survival in transplantation. Cytokines are reflected with immune responses. In the present study, we aimed to evaluate potential affecting factors of liver allograft survival and their possible correlation with seroum cytokine levels in living donor liver transplantation (LDLT). One hundred and seventy-one adult patients’ data were collected retrospectively. Five cytokines were collected: interferon (IFN)-γ, interleukin (IL)-2, IL-10, IL-6, and IL-17. Ischemic time of liver grafts was divided into two periods: cold and warm ischemic times (CIT and WIT, respectively). CIT had no statically significant correlation, but WIT showed a significant correlation with IFN-γ, IL-2, and IL-17 serum levels (r = 0.0252, 0.282, 0.178, respectively; P < 0.05). WIT was dichotomized as T1 (<22 min), T2 (22-70 min), and T3 (>70 min). IFN-γ was significantly increased in T2 and T3 as compared to T1. IL-6 was in T3 compared to T1 and T2. IL-17 was in T3 compared to T1. For the Th1-to-Th2 ratio, IFN-γ/IL-10, IFN-γ/IL-6, and IL-2/IL-10 were significantly different in T2 and T3 as compared to T1, and also in T3 as compared to T2. Th1 cell activities were enhanced with increased WIT. In conclusion, the longer WIT (>70 min) in LDLT is more likely to induce immunological reactions of recipients by leading to a deleterious cytokine balances in favor of an reinforced production of Th1 cytokines.

中文翻译：

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进行活体供体肝移植的患者中，移植肝的缺血时间迫使Th1-Th2活性朝Th1活性方向发展。

收件人的免疫反应是移植同种异体移植存活的重要因素。细胞因子通过免疫反应反映出来。在本研究中，我们旨在评估活体供肝移植（LDLT）中肝同种异体移植物存活的潜在影响因素及其与血清细胞因子水平的可能相关性。回顾性收集了一百七十一名成人患者的数据。收集了五种细胞因子：干扰素（IFN）-γ，白介素（IL）-2，IL-10，IL-6和IL-17。肝移植物的缺血时间分为两个时期：冷和热缺血时间（分别为CIT和WIT）。CIT没有静态的显着相关性，但是WIT与IFN-γ，IL-2和IL-17血清水平有显着相关性（r分别为0.0252、0.282、0.178；P <0.05）。将WIT分为T1（<22分钟），T2（22-70分钟）和T3（> 70分钟）。与T1相比，T2和T3中的IFN-γ显着增加。与T1和T2相比，IL-6在T3中。与T1相比，IL-17在T3中。对于Th1与Th2的比率，与T1相比，T2和T3中的IFN-γ/ IL-10，IFN-γ/ IL-6和IL-2 / IL-10显着不同，并且在T3中与T2相比。随着WIT的增加，Th1细胞活性增强。总之，LDLT中较长的WIT（> 70分钟）更可能通过导致有害的细胞因子平衡而有利于增强Th1细胞因子的产生来诱导受体的免疫反应。