Abstract
T cell migration through extracellular matrix of the tissue is an important process in the development of inflammation. However, the mechanisms regulating this process are complex and still not well defined. In this study, we show that activation of human peripheral blood T cells with anti-CD3 mAb increases the mRNA and protein levels of the discoidin domain receptor 1 (DDR1), which is known to bind to collagens. Furthermore, our findings indicate that DDR1 is involved in the migration of activated T cells in three-dimensional (3D) collagen. Indeed, the use of a DDR1 blocking molecule (DDR1:Fc) reduced the capacity of anti-CD3-activated human T cells to migrate in 3D collagen, whereas a control immunoglobulin had no effect. As a control, the DDR1:Fc molecule did not interfere with the capacity of human T cells to migrate through fibronectin. Together these results suggest that DDR1 can represent an additional receptor regulating T cell movement in the tissues and therefore can contribute to the development of inflammatory diseases.