TLR2 and TLR4 silencing in CD14++ monocytes of these patients prevents Treg differentiation to Th1-like Tregs and thus IFN-γ secretion by Tregs of these patients (Figure 3), suggesting that autoimmunity is promoted by CD14++ monocytes predominantly through activation of inflammatory signaling pathways. This evidence concerns the gene CD14 and Autoimmunity.