Fig. 2From: Dendritic cell-mediated chronic low-grade inflammation is regulated by the RAGE-TLR4-PKCβ1 signaling pathway in diabetic atherosclerosisAGEs plus oxLDL further induced the maturation of DCs and activated certain signaling pathways. The oxLDL plus AGEs treatment increased the expression of CD83 and CD86 (a), in BMDCs, and also up-regulated expression of IFNγ and TNFα (b), which was demonstrated by ELISA. In conjunction with stimulation by oxLDL, AGEs induced a greater degree of the phosphorylation of IκB, NF-κB (c), IRAK4 (d), PKCα/β1/β2 (f), and the expression of RAGE (e). Values, mean ± SED; n = 3, *p < 0.05 vs. oxLDL group; oxLDL oxidized low density lipoprotein, AGEs advanced glycation end-products, TNFα Tumor necrosis factor alpha, IFNγ IFN gamma, NF-κB nuclear factor-κB, RAGE Receptor for advanced glycation end products, pPKC phosphorylated protein kinase C, TLR4 Toll-like receptor 4, IRAK4 Interleukin receptor associated kinase 4Back to article page