Russell M A, Morgan N G
Institute of Biomedical and Clinical Science; University of Exeter Medical School ; Exeter , Devon , UK.
Islets. 2014;6(3):e950547. doi: 10.4161/19382014.2014.950547.
Considerable efforts have been invested to understand the mechanisms by which pro-inflammatory cytokines mediate the demise of β-cells in type 1 diabetes but much less attention has been paid to the role of anti-inflammatory cytokines as potential cytoprotective agents in these cells. Despite this, there is increasing evidence that anti-inflammatory molecules such as interleukin (IL)-4, IL-10 and IL-13 can exert a direct influence of β-cell function and viability and that the circulating levels of these cytokines may be reduced in type 1 diabetes. Thus, it seems possible that targeting of anti-inflammatory pathways might offer therapeutic potential in this disease. In the present review, we consider the evidence implicating IL-4, IL-10 and IL-13 as cytoprotective agents in the β-cell and discuss the receptor components and downstream signaling pathways that mediate these effects.
人们已经投入了大量精力来了解促炎细胞因子介导1型糖尿病中β细胞死亡的机制，但对于抗炎细胞因子作为这些细胞潜在细胞保护剂的作用却关注较少。尽管如此，越来越多的证据表明，白细胞介素（IL）-4、IL-10和IL-13等抗炎分子可直接影响β细胞功能和活力，且1型糖尿病患者这些细胞因子的循环水平可能降低。因此，针对抗炎途径进行干预似乎有可能为这种疾病提供治疗潜力。在本综述中，我们考虑了将IL-4、IL-10和IL-13作为β细胞保护剂的相关证据，并讨论了介导这些作用的受体成分和下游信号通路。
