Toll-like receptor 4 and CD14 on BDCA1+ myeloid dendritic cell (TLR4/CD14 on BDCA1+ mDC)

Toll-like receptor 4 (TLR4) and CD14 are co-expressed on BDCA1 (CD1c)+ myeloid dendritic cells, a human dendritic cell subset specializing in pathogen recognition and initiation of adaptive immune responses. TLR4 serves as a pattern recognition receptor that detects bacterial lipopolysaccharide (LPS) and mediates inflammatory signaling, while CD14 assists in LPS delivery to TLR4, enhancing sensitivity to microbial components[3][4]. BDCA1+ mDCs expressing both TLR4 and CD14 can mature upon stimulation, present antigens, and polarize naïve T cells toward specific immune responses (e.g., Th1)[2][4]. In cancer and chronic inflammation, BDCA1+CD14+ dendritic cells acquire immunosuppressive properties, upregulating checkpoint molecules like PD-L1 and secreting IL-10, thereby dampening T cell proliferation and promoting tumor immune evasion[1][5][8]. Structurally, TLR4 is a transmembrane receptor of the innate immune system, while CD14 is mainly a GPI-anchored or soluble co-receptor. Their trafficking and interactions, particularly with the LPS/LBP/MD-2 pathway, are critical for immune activation and resolution[3]. Note on correctness: The query combines two targets (TLR4 and CD14) on a specified cell type. For structured data, “Toll-like receptor 4” (TLR4) and “CD14” should be listed separately as protein targets, with BDCA1+ myeloid dendritic cell as their cellular context.

Other names

TLR4 (Toll-like receptor 4)CD14 (Cluster of Differentiation 14)BDCA1+ DC (Blood dendritic cell antigen 1-positive dendritic cell)CD1c+ myeloid dendritic cellMyeloid dendritic cell (mDC), subset cDC2

TLR4 antagonists block LPS binding and TLR4-mediated inflammatory signaling - CD14 inhibitors disrupt LPS transfer to TLR4/MD-2 complex, dampening TLR4 activation - Immunomodulators act by enhancing or suppressing DC antigen presentation and T-cell activation