作者
Keum Hwa Lee,Andreas Kronbichler,David Duck-Young Park,Young Min Park,Hanwool Moon,Hyung Do Kim,Jun Hyug Choi,YoungSeo Choi,S. Shim,Il Suk Lyu,Byung Hwan Yun,Yeonseung Han,Dong-Hee Lee,Sang-Yoon Lee,Byung Hun Yoo,Kyung Hwan Lee,Tai Lim Kim,Heonki Kim,Joo Sung Shim,Won-Seok Nam,Heesung So,Soo-Yeon Choi,Sangmok Lee,Jae Il Shin
摘要
Neutrophil extracellular traps (NETs) are fibrous networks which protrude from the membranes of activated neutrophils. NETs are found in a variety of conditions such as infection, malignancy, atherosclerosis, and autoimmune diseases including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), psoriasis, and gout. Studies suggest that an imbalance between “NETosis,” which is a process by which NETs are formed, and NET degradation may be associated with autoimmune diseases. Neutrophils, interleukin-8, ANCA and other inflammatory molecules are considered to play a key role in NET formation. Prolonged exposure to NETs-related cascades is associated with autoimmunity and increases the chance of systemic organ damage. In this review, we discuss the roles of various inflammatory molecules in relation to NETs. We also describe the role of NETs in the pathogenesis of autoimmune diseases and discuss the possibility of using targeted therapies directed to NETs and associated molecules to treat autoimmune diseases.