Human IL-23R Cytokine-Binding Homology Region-Fc Fusion Protein Ameliorates Psoriasis via the Decrease of Systemic Th17 and ILC3 Cell Responses
Human IL-23R Cytokine-Binding Homology Region-Fc Fusion Protein Ameliorates Psoriasis via the Decrease of Systemic Th17 and ILC3 Cell Responses
复制标题
人 IL-23R 细胞因子结合同源区 Fc 融合蛋白通过减少全身 Th17 和 ILC3 细胞反应来改善银屑病
DOI：
10.3390/ijms20174170
复制
发表时间：
2019-09-01
影响因子：
5.6
通讯作者：
Guo, Wei
中科院分区：
文献类型：
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作者：
Gao, Yue;Bian, Zhengying;Guo, Wei
由于IL-23/IL-17轴在银屑病发病机制中的关键作用，白细胞介素（IL）-23被认为是治疗银屑病的有效治疗靶点，并且最近报道其参与ILC 3细胞分化。在这项研究中，我们报告，真核表达的rhIL 23 R-Fc/Fc，作为一种内源性细胞外受体类似物，可以是一种天然的拮抗剂在咪喹莫特（IMQ）诱导的银屑病样小鼠模型，包括拮抗作用的抑制炎症的皮肤病变，减少生产的促炎细胞，并减少促炎因子的表达。rhIL 23 R-Fc/Fc融合蛋白抑制先天性免疫和适应性免疫介导的炎症反应。这些发现揭示了rhIL 23 R-Fc/Fc作为治疗银屑病的有希望的候选疗法。
Interleukin (IL)-23 is considered an effective therapeutic target for the treatment of psoriasis because of the crucial role of the IL-23/IL-17 axis in the pathogenesis of psoriasis, and it has recently been reported to be involved in ILC3 cell differentiation. In this study, we report that eukaryotically expressed rhIL23R-CHR/Fc, as an endogenous extracellular receptor analogue, could be a natural antagonist in an imiquimod (IMQ)-induced psoriasis-like mouse model, including the antagonizing effect of suppressed inflammation in the skin lesion, decreased production of pro-inflammatory cells, and reduced the expression of pro-inflammatory factors. The rhIL23R-CHR/Fc fusion protein inhibits both innate immune and adaptive immune-mediated inflammatory responses. These findings shed light on rhIL23R-CHR/Fc as a promising candidate therapy for the treatment of psoriasis.