IL-17 Contributes to the Development of Chronic Rejection in a Murine Heart Transplant Model
IL-17 Contributes to the Development of Chronic Rejection in a Murine Heart Transplant Model
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DOI：
10.1007/s10875-009-9366-9
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发表时间：
2010-03-01
影响因子：
9.1
通讯作者：
Fischbein, Michael P.
中科院分区：
文献类型：
--
作者：
Itoh, Satoshi;Nakae, Susumu;Fischbein, Michael P.
虽然白细胞介素-17（IL-17）已被报道参与感染性、自身免疫性和过敏性疾病的发病机制，但其在同种异体移植排斥反应中的确切作用仍不清楚。利用小鼠异位心脏移植模型系统，IL-17缺陷的受体小鼠减少了同种异体移植物炎性细胞的募集，减少了IL-6、MCP-1和KC的产生，并减少了移植物冠状动脉疾病（GCAD）。移植物内γ δ（γ δ）T细胞似乎是产生IL-17的主要来源，因此，IL-17中和可能为心脏移植排斥反应的治疗提供一个潜在的靶点。
Although interleukin-17 (IL-17) has been reported to participate in the pathogenesis of infectious, autoimmune and allergic disorders, the precise role in allograft rejection remains uncertain. This study illustrates that IL-17 contributes to the pathogenesis of chronic allograft rejection.Utilizing a murine heterotopic heart transplant model system, IL-17-deficient recipient mice had decreased allograft inflammatory cell recruitment, decreased IL-6, MCP-1, and KC production, and reduced graft coronary artery disease (GCAD). Intragraft gamma delta (gamma delta) T cells appear to be the predominant source of IL-17 production.Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.