SLC/CCR7 stimulates the proliferation of BMDCs by the pNF-kappaB p65 pathway

Abstract

The chemokine receptor CCR7 is highly expressed in dendritic cells (DCs), T cells, and other immune effector cells. One of the high-affinity ligand that can bind to CCR7 is the secondary lymphoid tissue chemokine (SLC). The SLC/CCR7 axis plays an important role in the immune system by inducing the chemotaxis and migration of immune effector cells. In this study, we examined the effect of SLC at different concentrations (0, 50, 100, 200, 300, and 400 ng/mL) on the proliferation of bone-marrow-derived dendritic cells (BMDCs). ELC (CCL19), another high-affinity ligand for CCR7, was used as the control at the same time. We found that SLC directly stimulated the proliferation of BMDCs and enhanced the antigen-presenting function and CCR7 expression. Western blot analysis showed that pNF-kappaBp65 was involved in this mechanism. We also found that the NF-kappaB inhibitor PDTC could specifically block the proliferation and CCR7 expression of BMDCs induced by SLC or ELC (200 ng/mL). The results suggested that there were cross-talk signals between the chemotaxis and proliferation of BMDCs involving the SLC/CCR7 axis.