Redox-Dependent Inflammation in Islet Transplantation Rejection.

Redox-Dependent Inflammation in Islet Transplantation Rejection.
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DOI:
10.3389/fendo.2018.00175
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发表时间:
2018
影响因子:
5.2
通讯作者:
Tse HM
Tse HM
中科院分区:
医学2区
文献类型:
--
作者:
Barra JM;Tse HM

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1 型糖尿病是一种自身免疫性疾病,会导致胰岛内产生胰岛素的胰腺 β 细胞逐渐遭到破坏。这一重要群体的丧失使患者终生依赖外源性胰岛素,并使他们面临危及生命的并发症的风险。正在研究的一种帮助这些患者恢复胰岛素独立性的方法是胰岛细胞移植。然而,与移植排斥和胰岛活力相关的挑战阻碍了β细胞的长期功能。氧化还原信号传导以及受体免疫细胞和移植胰岛本身产生的活性氧 (ROS) 是移植排斥的关键因素。因此,消除ROS的产生是一种可行的干预措施,可以保护移植的胰岛免受免疫介导的破坏。在这里,我们将讨论氧化还原信号传导和 ROS 合成在移植排斥过程中新近认识到的作用,以及正在测试其在胰岛细胞移植过程中氧化还原调节功效的新策略。
Type 1 diabetes is an autoimmune disease that results in the progressive destruction of insulin-producing pancreatic β-cells inside the islets of Langerhans. The loss of this vital population leaves patients with a lifelong dependency on exogenous insulin and puts them at risk for life-threatening complications. One method being investigated to help restore insulin independence in these patients is islet cell transplantation. However, challenges associated with transplant rejection and islet viability have prevented long-term β-cell function. Redox signaling and the production of reactive oxygen species (ROS) by recipient immune cells and transplanted islets themselves are key players in graft rejection. Therefore, dissipation of ROS generation is a viable intervention that can protect transplanted islets from immune-mediated destruction. Here, we will discuss the newly appreciated role of redox signaling and ROS synthesis during graft rejection as well as new strategies being tested for their efficacy in redox modulation during islet cell transplantation.
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