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IL-36 family cytokines in protective versus destructive inflammation

机译：IL-36保护性与破坏性炎症的家庭细胞因子

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摘要

The IL-1 family of cytokines and receptors are critical regulators of inflammation. Within the IL-1 family and in contrast to its IL-1 and IL-18 subfamilies, the IL-36 subfamily is still poorly characterized. Three pro-inflammatory agonists IL-36 alpha, IL-36 beta, IL-36 gamma, one IL-36 receptor (IL-1R6) antagonist, IL-36RA, and one putative IL-1R6 antagonist, IL-38, have been grouped into the IL-36 cytokine subfamily. IL-36 agonists signal through a common receptor complex to serve as early triggers of inflammatory responses by activating and cross-regulating a number of inflammatory pathways including NF-KB, MAPK and IFN signaling. IL-36RA binds to IL-1R6 to limit inflammatory signaling, while IL-38 may be an antagonist of more than one IL-1 family receptor. Expression patterns of IL-36 family cytokines, being most prominently expressed in epithelial barrier tissues such as the skin and intestines as well as in immune cells, suggest a role in protecting these barriers from infection. Dysregulation of IL-36 family cytokine signaling at physiological barriers, most prominently the skin, induces autoimmune inflammation. However, transferring the potential of IL-36 to induce tissue damage to tumors might benefit cancer patients. Here we summarize signaling pathways regulated by IL-36 family cytokines, including IL-38, and the consequences for physiological protective and pathophysiological destructive inflammation. Moreover, we discuss the limits of current knowledge on IL-36 family function to open potential avenues for research in the future.
机译：IL-1家族细胞因子和受体是炎症的关键调节因子。在IL-1家族内，与其IL-1和IL-18亚属植物相比，IL-36亚家族的特征仍然很差。三个促炎激动剂IL-36α，IL-36β，IL-36γ，一个IL-36受体（IL-1R6）拮抗剂，IL-36ra和一个推定的IL-1R6拮抗剂，IL-38已经存在分组成IL-36细胞因子亚家族。 IL-36激动剂通过普通受体络合物发出通过激活和交叉调节包括NF-KB，MAPK和IFN信号传导的许多炎性途径作为炎性反应的早期触发。 IL-36ra与IL-1R6结合以限制炎症信号传导，而IL-38可以是多于一个IL-1家族受体的拮抗剂。 IL-36家族细胞因子的表达模式最突出地在上皮阻隔组织中表达，例如皮肤和肠以及免疫细胞，表明保护这些障碍免受感染的作用。 IL-36家族细胞因子信号在生理障碍，最突出的皮肤，诱导自身免疫性炎症。然而，转移IL-36的潜力诱导肿瘤的组织损伤可能会使癌症患者受益。在这里，我们总结了由IL-36家族细胞因子调节的信号通路，包括IL-38，以及对生理保护和病理生理破坏性炎症的后果。此外，我们讨论了当前关于IL-36家族功能知识的限制，以便将来开放潜在的途径。

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  • 来源
    《Cellular Signalling》 |2020年第1期|共13页
  • 作者

    Han Yingying; Huard Arnaud; Mora Javier; da Silva Priscila; Bruene Bernhard; Weigert Andreas;

  • 作者单位

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

    Goethe Univ Frankfurt Fac Med Inst Biochem 1 D-60590 Frankfurt Germany;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞形态学;
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