IL-33/ST2-mediated inflammation in macrophages is directly abrogated by IL-10 during rheumatoid arthritis

作者：Si Chen, Bingni Chen, Zhongyang Wen, Zhong Huang, Liang Ye · 发表于：Oncotarget · 年份：2017 · DOI：10.18632/oncotarget.16299 · 被引用次数：46 · 研究领域：IL-33, ST2, and ILC Pathways、Eosinophilic Esophagitis、Inflammatory Bowel Disease

// Si Chen 1,2,* , Bingni Chen 1,2,3,* , Zhongyang Wen 1,2,3,* , Zhong Huang 1,2,3 and Liang Ye 1,2,3 1 Institute of Biological Therapy, Shenzhen University, Shenzhen, China 2 Department of Pathogen Biology and Immunology, Shenzhen University School of Medicine, Shenzhen, China 3 Shenzhen City Shenzhen University Immunodiagnostic Technology Platform, Shenzhen, China * These authors have contributed equally to this work Correspondence to: Liang Ye, email: // Zhong Huang, email: // Keywords : IL-33, IL-33 receptor, IL-10, macrophage, rheumatoid arthritis, Immunology and Microbiology Section, Immune response, Immunity Received : August 11, 2016 Accepted : March 01, 2017 Published : March 16, 2017 Abstract IL-10 is an immunosuppressive cytokine produced and sensed by many immune cells and exerts a protective role in autoimmune diseases. However, the underlying mechanism by which IL-10 contributes to prevent the arthritic inflammation in macrophages is poorly understood. Herein we report on a novel anti-arthritic property of IL-10 through the inhibition of IL-33 signaling by macrophages during collagen-induced arthritis (CIA) development. We show that IL-33 expression rather than its receptor (ST2) is positively correlated with IL-10 level in active RA. IL-10 deficiency in mice leads to significant upregulation of IL-33 expression and aggravates the progression of CIA, while exogenous IL-10 treatment effectively diminishes IL-33 production in IL-10 knockout (IL-10 -/- ) CIA mice. ...