IL-17A exacerbates psoriasis in a STAT3 overexpressing mouse model

PeerJ

article

Xinran Xie¹  Lei Zhang¹  Yan Lin¹  Xin Liu¹  Ning Wang¹  Ping Li¹ 

[1] Beijing Hospital of Traditional Chinese Medicine, Capital Medical University;Beijing Institute of Chinese Medicine

关键词: Psoriasis;    IL-17A;    STAT3;    Bioinformatics;    Mouse model;   

DOI  :  10.7717/peerj.15727

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Background Psoriasis is an autoimmune skin disease characterized by immunocyte activation, excessive proliferation, and abnormal differentiation of keratinocytes. Signal transducers and activators of transcription 3 (STAT3) play a crucial role in linking activated keratinocytes and immunocytes during psoriasis development. T helper (Th) 17 cells and secreted interleukin (IL)-17A contribute to its pathogenesis. IL-17A treated STAT3 overexpressing mouse model might serve as an animal model for psoriasis. Methods In this study, we established a mouse model of psoriasiform dermatitis by intradermal IL-17A injection in STAT3 overexpressing mice. Transcriptome analyses were performed on the skin of wild type (WT), STAT3, and IL-17A treated STAT3 mice. Bioinformatics-based functional enrichment analysis was conducted to predict biological pathways. Meanwhile, the morphological and pathological features of skin lesions were observed, and the DEGs were verified by qPCR. Results IL-17A treated STAT3 mice skin lesions displayed the pathological features of hyperkeratosis and parakeratosis. The DEGs between IL-17A treated STAT3 mice and WT mice were highly consistent with those observed in psoriasis patients, including S100A8, S100A9, Sprr2, and LCE. Gene ontology (GO) analysis of the core DEGs revealed a robust immune response, chemotaxis, and cornified envelope, et al. The major KEGG enrichment pathways included IL-17 and Toll-like receptor signaling pathways. Conclusion IL-17A exacerbates psoriasis dermatitis in a STAT3 overexpressing mouse.

【 授权许可】

CC BY