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. 2018 Mar 19;9:559. doi: 10.3389/fimmu.2018.00559

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Copyright © 2018 Chen, Wang, Li, Yu, Chen and Zhao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A proposed model of factor H (FH)–neutrophil interaction in the pathogenesis of anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV). (A) TNF/β2-integrin joint signals triggers explosive responses of neutrophils adherent to endothelial cells in the presence of ANCA, resulting in degranulation and oxidative burst of neutrophils. (B) Binding of FH on neutrophils through β2-integrin inhibits ANCA-induced activation of neutrophils. (C) In AAV, FH is deficient in binding neutrophils and inhibiting neutrophil activation by ANCA, which may be partly related to tyrosine nitration and chlorination of FH and genetic variations of FH.