排斥反应是阻碍心脏移植患者术后长期存活的主要因素, 如何有效安全的预防排斥反应是目前心脏移植研究的难点和热点。细胞因子作为排斥反应中的关键分子，介导并调控免疫应答的类型与强弱。JAK/STAT是近来发现的重要的细胞因子信号通路, 介导白介素、干扰素、集落刺激因子、生长激素等众多细胞因子效应，参与免疫活化及效应全过程。 以往研究表明,通过对该通路的调节可能影响免疫反应的方向和强度。SOCS是重要内源调控因子，广泛存在于各种细胞中，通过抑制JAK／STAT通路发挥负向调节功能。研究表明SOCS3在多种炎性疾病中发挥抗炎作用，但其对排斥反应的作用不明确。本研究拟采用腺病毒载体、基因敲除小鼠模型等方法探讨其对免疫细胞影响，明确其在心脏移植排斥反应中的作用机制。鉴于负向调控机制的在免疫反应中的重要作用，本研究结果可能为排斥反应的防治提供新的思路。

Allograft rejection is main obstacle for long survival after cardiac transplantation. Cytokines are key molecules which modulate the intensity and duration of immune response during rejection. Janus kinase/signal transducers and activators of transcription (JAK/STAT) is an important cytokine signal pathway which mediates the signaling of a number of cytokines such as interleukins, interferons, hemopoietin, colony stimulating factors and growth hormone, it plays a critical role in activation and effcts of immune response, privious studies suggested regualtion of JAK/STAT pathway may modulate the type and intensity of immune response. Suppressor of cytokine signaling (SOCS) proteins are potential endogenous negative regulators of JAK/STAT and express in various kinds of cells. Growing body of evidences suggests that SOCS3 plays an anti-inflammatory role in large number of inflammatory diseases. However, the involvement of SOCS3 in allograft rejection still remains to be understood. The purpose of this project is to study the effects and associative mechanisms of SOCS3 on allograft rejection both in vitro and in vivo by using gene transfection and cardiac transplantation model in conditional SOCS3 knockout mouse. As to the essential role of endogenous negative regulator on the immune response,the results of this study may provide a novelty strategy of clinical treatment for transplantation rejection.