| First Author | Lee JE | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 352 |
| Issue | 1 | Pages | 244-50 |
| PubMed ID | 17113033 | Mgi Jnum | J:116601 |
| Mgi Id | MGI:3694568 | Doi | 10.1016/j.bbrc.2006.11.010 |
| Citation | Lee JE, et al. (2007) Discoidin domain receptor 2 is involved in the activation of bone marrow-derived dendritic cells caused by type I collagen. Biochem Biophys Res Commun 352(1):244-50 |
| abstractText | 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. |
