Source:Autoimmunity Reviews
Author(s): Keum Hwa Lee, Andreas Kronbichler, David Duck-Young Park, YoungMin Park, Hanwool Moon, Hyungdo Kim, Jun Hyug Choi, YoungSeo Choi, Songjoo Shim, Il Suk Lyu, Byung Hwan Yun, Yeonseung Han, Donghee Lee, Sang Yoon Lee, Byung Hun Yoo, Kyung Hwan Lee, Tai Lim Kim, Heonki Kim, Joo Sung Shim, Wonseok Nam, Heesung So, SooYeon Choi, Sangmok Lee, Jae Il Shin
The structures named neutrophil extracellular traps (NETs) are fibrous networks which protrude from the membrane of activated neutrophils. NETs are found in a variety of conditions, such as infection, malignancy, atherosclerosis, and autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), psoriasis, and gout. The impact of NETs on the development mechanisms of autoimmune diseases are proposed to arise from an imbalance between "NETosis" which is a process of NET formation and NET degradation. Neutrophils, interleukin-8, ANCA and other many inflammatory molecules are considered to play a key role in NET formation. In this way, prolonged exposure to these abnormal cascade of NETs affect autoimmunity and increase the chance of systemic organ damage. In this review, we will discuss the specific roles of various inflammatory molecules in relationship to NETs. We will also provide evidence of the importance of NETs in the pathogenesis of autoimmune diseases and furthermore highlight the potential that target therapies may influence NET formation and associated molecules.
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