C5a/C5aR1 mediates IMQ‐induced psoriasiform skin inflammation by promoting IL‐17A production from γδ‐T cells

• Published in: The FASEB journal Vol. 34; no. 8; pp. 10590 - 10604
• Main Authors: Zheng, Quan‐you, Xu, Feng, Yang, Yi, Sun, Dao‐dong, Zhong, Yu, Wu, Shun, Li, Gui‐qing, Gao, Wei‐wu, Wang, Tao, Xu, Gui‐lian, Liang, Shen‐ju
• Format: Journal Article
• Language: English
• Published: United States 01.08.2020
• Subjects: Animals; C5a; C5aR1; complement system; Cytokines - metabolism; Down-Regulation - drug effects; Down-Regulation - genetics; Female; Gene Expression - drug effects; Gene Expression - physiology; imiquimod; Imiquimod - pharmacology; Inflammation - drug therapy; Inflammation - metabolism; Interleukin-17 - metabolism; Intraepithelial Lymphocytes - drug effects; Intraepithelial Lymphocytes - metabolism; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Phosphatidylinositol 3-Kinases - metabolism; PI3K‐Akt signaling; Proto-Oncogene Proteins c-akt - metabolism; Psoriasis - drug therapy; Psoriasis - metabolism; Receptor, Anaphylatoxin C5a - metabolism; Signal Transduction - drug effects; Signal Transduction - physiology; Skin - drug effects; Skin - metabolism; γδ‐T cells; PI3K-Akt signaling; complement system; C5a; C5aR1; imiquimod; γδ-T cells

Psoriasis is a chronic relapsing inflammatory skin disease, affecting up to 3% of the global population. Accumulating evidence suggests that the complement system is involved in its pathogenesis. Our previous study revealed that the C5a/C5aR1 pathway is crucial for disease development. However, the...