HMGB1 is involved in chronic rejection of cardiac allograft via promoting inflammatory-like mDCs.

摘要: Chronic rejection that leads to diffuse narrowing and occlusion of graft vessels is the most important cause morbidity mortality following cardiac transplantation. The role underlying mechanism high-mobility group box 1 (HMGB1), as an established inflammatory mediator in acute rejection, remains poorly understood chronic rejection. Here, we assessed effects mechanisms HMGB1 on using single MHC Class II-mismatched mouse transplantation model. It was found increased accompanying with development while blockade specific neutralizing mAb substantially ameliorated rejection-mediated vasculopathy fibrosis allograft, well markedly decreased T cell infiltration production IL-17A interferon-gamma allograft recipient's spleen. Further, anti-HMGB1 antibody treatment significantly declined number frequency mature dendritic cells (DCs) spleen, especially CD11b(+) Ly6C(high) matured DCs share phenotypes inflammatory-DCs. These findings indicate contributes may be a novel mean disrupt proinflammatory loop after heart