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Neutralization of IL-17 inhibits the production of anti-ANT autoantibodies in CVB3-induced acute viral myocarditis

Anti-adenine nucleotide translocator (ANT) autoantibodies are related to the development of Coxsackievirus B3 (CVB3)-triggered acute viral myocarditis (AVMC). Recently, studies suggested that IL-17 especially produced by a novel CD4 + Th-cell subset Th17 cells contributed to the production of pathog...

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Published in:International immunopharmacology 2010-03, Vol.10 (3), p.272-276
Main Authors: Yuan, Jing, Yu, Miao, Lin, Qiong-Wen, Cao, Ai-Lin, Yu, Xian, Dong, Ji-Hua, Wang, Jin-Ping, Zhang, Jing-Hui, Wang, Min, Guo, He-Ping, Liao, Yu-Hua
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Language:English
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Summary:Anti-adenine nucleotide translocator (ANT) autoantibodies are related to the development of Coxsackievirus B3 (CVB3)-triggered acute viral myocarditis (AVMC). Recently, studies suggested that IL-17 especially produced by a novel CD4 + Th-cell subset Th17 cells contributed to the production of pathogenic autoantibodies in some autoimmune diseases. However, the pathogenic role of IL-17 in AVMC remains largely unknown. In this study, we investigated whether IL-17 was associated with the disease progression and the production of anti-ANT autoantibodies in AVMC mouse model. The results showed that IL-17 monoclonal antibody (mAb)-treated AVMC mice had decreased HW/BW, reduced serum CK-MB activity and improved pathological score of heart sections along with the reduction of circulating IL-17 level and serum anti-ANT autoantibodies. The correlation index of serum IL-17 concentration and anti-ANT-autoantibody level was 0.874, p < 0.01. In addition, the experimental results in vitro further proved that IL-17mAb could inhibit the proliferation of CD19 + B lymphocytes and the secretion of anti-ANT autoantibodies. Our data suggested that IL-17 was related to the disease progression in AVMC mouse model by regulating the production of autoantibodies and blocking IL-17 might represent a promising novel therapeutic approach.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2009.11.010