HMGB1 and lupus nephritis: TLR2 and TLR4 were both suggested to be receptors for HMGB1 in a study by Park et al. in 2004 (Park et al. 2004) and since, the TLR2-HMGB1 axis has been suggested to contribute to the pathogenesis of several conditions including myocardial ischemia/reperfusion injury, peripheral artery disease, deep venous thrombosis and lupus nephritis (Stark et al. 2016; Feng et al. 2016; Mersmann et al. 2013; Sachdev et al. 2012; Xu et al. 2015).