The activation of bone marrow‐derived dendritic cells is enhanced by type I collagen through discoidin domain receptor‐2

Dendritic cells (DCs) are the most central player in the initiation and direction of immune responses as effective antigen‐presenting cells. It remains still to understand whether Discoidin domain receptors (DDRs), which are non‐integrin‐type receptor tyrosine kinases for collagen on many cell types, can regulate the activation of DCs by collagen. In this study, we investigated the contributions of DDRs on the maturation and activation of mouse bone marrow‐derived dendritic cells (DCs) by type I collagen (ColI). We observed that transcripts and proteins of DDR2 were expressed constitutively in bone marrow‐derived immature DCs during development and upregulated in TNF‐alpha‐stimulated DCs. In addition, ColI treatment induced DDR2 phosphorylation and subsequently augmented IL‐12 production, CD86 expression, antigen uptake activity, and allogeneic mixed T cell reaction by immature DCs. Depletion of DDR2 by specific siRNA reduced significantly the functional activity of DCs upregulated by ColI. These results suggest that DDR2‐collagen interaction may play an important role in the functional capacity of DCs regulating immune responses.