Human IL-23R Cytokine-Binding Homology Region-Fc Fusion Protein Ameliorates Psoriasis via the Decrease of Systemic Th17 and ILC3 Cell Responses

International Journal of Molecular Sciences

Qianwen Li¹  Lei Tang¹  Wenyao Xue¹  Wei Guo¹  Zhengying Bian¹  Yu Zeng¹  Yimeng Wang¹  Yue Gao¹  Tiejun Tang¹  Xiangdong Gao¹ 

[1] Jiangsu Key Laboratory of Druggability of Biopharmaceuticals and State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China;

关键词: psoriasis;    IL-23/IL-17 axis;    Th17 cells;    adaptive immunity;    innate immune;   

DOI  :  10.3390/ijms20174170

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown