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Lee, J.E. et al.

Discoidin domain receptor 2 is involved in the activation of bone marrow-derived dendritic cells caused by type I collagen.

Discoidin domain receptors (DDRs), DDR1 and DDR2, are non-integrin receptor tyrosine kinases for collagen in many cell types. In this study, we investigated the contributions of DDRs to the activation of mouse bone marrow-derived dendritic cells (DCs) by type I collagen (ColI). Our data showed that transcript and protein of DDR2 were expressed constitutively in immature DCs and upregulated in TNF-alpha-stimulated mature DCs. ColI treatment induced DDR2 phosphorylation and subsequently induced the upregulation of IL-12 production, CD86 expression, and antigen uptake activity by immature DCs. Depletion of DDR2 by specific siRNA attenuated significantly an increase in expression of IL-12 and CD86 in ColI-treated DCs. Additionally, DDR2-ColI interaction upregulated the ability of mature DCs to activate allogeneic T cells. These findings suggest that DDR2 is a critical collagen receptor for DC activation and that DDR2-collagen interaction plays an important role in the functional capacity of DCs regulating immune responses.[1]

References

Discoidin domain receptor 2 is involved in the activation of bone marrow-derived dendritic cells caused by type I collagen. Lee, J.E., Kang, C.S., Guan, X.Y., Kim, B.T., Kim, S.H., Lee, Y.M., Moon, W.S., Kim, D.K. Biochem. Biophys. Res. Commun. (2007) [Pubmed]

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