Collagen I enhances functional activities of human monocyte-derived dendritic cells via discoidin domain receptor 2

We evaluated the involvement of collagen and their discoidin domain receptors (DDRs), DDR1 and DDR2, on the activation of human monocyte-derived dendritic cells (hDCs). DDR2 was markedly expressed on mature hDCs in comparison to immature ones. Collagen I enhanced the release of IL-12p40, TNF-α and IFN-γ by hDCs. Additionally, hDCs exhibited enhanced expression of costimulatory molecules, and potent functional activities which, in turn, has therapeutic value. Interestingly, DDR2 depletion showed decrease in capacity of hDCs to stimulate T cells proliferation, whereas DDR1 silencing had no significant affect. These data demonstrate that DDR2 enhances hDCs activation and contributes to their functional activities. In addition, application of collagen I treated dendritic cells (DCs) vaccine reduced tumor burden giving longer survival in melanoma mice. Our study suggests that collagen I may enhance functional activities of DCs in immune response.

► Role of collagen I and discoidin domain receptors (DDRs) on function of human monocyte-derived DCs was evaluated.
► Collagen I-human monocyte-derived dendritic cells (hDCs) upregulated release of cytokines and expression of costimulatory molecules.
► Depletion of DDR2 suppressed the functional ability of hDCs to proliferate T cells.
► Collagen I treated DCs reduced tumor burden in melanoma mice giving longer survival.
► Collagen I may enhance functional activities of DCs in immune response.