IL-17 upregulates MCP-1 expression via Act1 / TRAF6 / TAK1 in experimental autoimmune myocarditis
Xiao Huang 1 , Zhuolun Li 2 , Xinhe Shen 1 , Na Nie 1 , Yan Shen 3 Affiliations
- PMID: 35183823
- DOI: 10.1016/j.cyto.2022.155823
- Corrigendum to “IL-17 upregulates MCP-1 expression via Act1/TRAF6/TAK1 in experimental autoimmune myocarditis” [Cytokine 152 (2022) 155823]. Huang X, Li Z, Shen X, Nie N, Shen Y. Cytokine. 2022 Apr 9;154:155879. doi: 10.1016/j.cyto.2022.155879. Online ahead of print. PMID: 35413623 No abstract available.
Myocarditis is a kind of myocardial inflammatory infiltration disease. Many interventions are not effective in the treatment of myocarditis because the mechanism of myocarditis has not been elucidated. Previous studies have found that interleukin-17 (IL-17) could stimulate the expression of monocyte chemokine protein 1 (MCP-1) and mediate myocardial inflammatory infiltration. This study aimed to explore the role of Act1/TRAF6/TAK1 cascade in IL-17-induced MCP-1 expression based on a well-designed experimental autoimmune myocarditis (EAM) model. It was found that IL-17 could stimulate the expression of MCP-1 by activating Act1/TRAF6/TAK1 cascade in EAM. The expression of Act1, TRAF6 and TAK1 followed downregulation by the application of IL-17 antibody. Additionally, myocardial inflammatory cell infiltration was observably alleviated by interfering TAK1 with TAK1 siRNA, and both MCP-1 mRNA and protein expression followed downregulation. This study suggested that IL-17 could activate the Act1/TRAF6/TAK1 pathway to upregulate MCP-1 expression in the EAM, and will offer a new perspective for the study on the mechanism of myocarditis.
Keywords: Act1/TRAF6/TAK1 cascade; Experimental autoimmune myocarditis; Interleukin-17; Monocyte chemokine protein 1.