IL-17 有助于小鼠心脏移植模型中慢性排斥反应的发展。
IL-17 contributes to the development of chronic rejection in a murine heart transplant model.
机构信息
Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
出版信息
J Clin Immunol. 2010 Mar;30(2):235-40. doi: 10.1007/s10875-009-9366-9. Epub 2010 Feb 4.
BACKGROUND
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.
RESULT
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 (gammadelta) T cells appear to be the predominant source of IL-17 production.
CONCLUSION
Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.
背景
尽管白细胞介素-17（IL-17）已被报道参与感染、自身免疫和过敏疾病的发病机制，但它在同种异体移植排斥反应中的确切作用仍不确定。本研究表明，IL-17 有助于慢性同种异体移植排斥反应的发病机制。
结果
利用小鼠异位心脏移植模型系统，IL-17 缺陷型受体小鼠的同种异体移植物炎性细胞募集减少，IL-6、MCP-1 和 KC 的产生减少，移植物冠状动脉疾病（GCAD）减少。同种异体移植内的γδ（γδ）T 细胞似乎是 IL-17 产生的主要来源。
结论
因此，IL-17 中和可能为心脏同种异体移植排斥的新型治疗提供潜在的治疗靶点。
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