Fig. 12

A schematic summary of the latest evidence and experimental results in this study. Under the specific intra-pulmonary cytokine milieu with increased IL-6 expression in SLE-AH lung tissues, upregulated SNHG16 levels in alveolar cells and resident neutrophils can enhance TLR4 expression via stabilizing its mRNA expression and sponging miRNAs that can target it, e.g. miR-146a. TRAF6, a miR-146a target molecule, is a potent inducer of autophagy and NETosis. TRAF6, a miR-146a target molecule, is an inducer of autophagy and NETosis. SNHG16 can regulate the TLR4/TRAF6 axis and activate downstream genes to generate pro-inflammatory cytokines like IL-8, a potent inducer of NETosis. Under high ROS levels, the autophagic process is initiated through the inactivation of mTOR pathway. Figure is created with BioRender.com