For example, the expression levels of TLR2 and TLR4 mRNAs in SLE patients’ PBMCs are much higher than those in healthy subjects [31], and the expression of TLR3 mRNA increases with the progression of lupus nephritis [32, 33] while downregulation of TLR2 or TLR4 can decrease the production of autoantibodies and attenuates the development of renal injury in lpr mutation-induced murine lupus[34]. This evidence concerns the gene TLR4 and lupus nephritis.