
IndraLab
Statements
sparser
"Studies have showed that after anthracyclines treatment of NSCLC tumor cells, calreticulin (CALR) on the cell membrane interacts with its own receptor TLR4 to activate the CALR-TLR4-MyD88 signaling pathway, phosphorylating NF-κB, JNK, ERK, p38 MAPK and other signaling pathways. xref , xref Subsequently secreted C-C motif chemokine ligand 19 (CCL19) and TNF-α promote the migration and maturation of imDCs, ultimately inhibiting NSCLC progression. xref In mouse lung cancer models, S. Hillinger et al identified CCL19 as a potential immune stimulator that significantly increases DCs in the lung. xref In addition, TNF-α exhibits strong inflammatory and tumor-promoting properties and can influence tumor progression through complex signal transduction phenomena, including NF-κB, MAPK, AKT, etc. xref A study revealed that CD34 + /CD86 + cells, common precursors for macrophages and DCs, differentiate into macrophages when cultured with granulocyte-macrophage colony-stimulating factor (GM-CSF)."
reach
"Calreticulin, ATP, and HMGB1 bind to CD91, P2RX7, and TLR4, respectively, facilitating dendritic cell (DC) recruitment into the tumor bed (by ATP), the phagocytosis of tumor antigens by DCs (enhanced by CRT), and an optimal antigen presentation to T cells (stimulated by calreticulin and HMGB1)."