Related Experiment Video
Updated: Jul 18, 2026

Generation of Bone Marrow Derived Murine Dendritic Cells for Use in 2-photon Imaging
Published on: July 9, 2008
Discoidin domain receptor 2 is involved in the activation of bone marrow-derived dendritic cells caused by type I
Ji-Eun Lee1, Chon-Sik Kang, Xiu-Ying Guan
1Department of Immunology, Chonbuk National University Medical School, Jeonbuk 561-180, Republic of Korea.
Abstract:
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.
Insights
Discoidin domain receptor 2 (DDR2) is crucial for activating mouse dendritic cells (DCs) by collagen. DDR2 signaling enhances DC functions, impacting immune responses.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Discoidin domain receptors (DDRs) are receptor tyrosine kinases that bind collagen.
- Dendritic cells (DCs) are key antigen-presenting cells in the immune system.
Purpose of the Study:
- To investigate the role of DDRs, specifically DDR2, in the activation of mouse bone marrow-derived dendritic cells (DCs) by type I collagen (ColI).
Main Methods:
- Analysis of DDR2 expression in immature and mature DCs.
- Treatment of DCs with ColI and assessment of DDR2 phosphorylation.
- Evaluation of DC activation markers (IL-12, CD86) and functions (antigen uptake, T cell activation).
- DDR2 depletion using siRNA.
Main Results:
- DDR2 is constitutively expressed in immature DCs and upregulated in mature DCs.
- ColI treatment phosphorylates DDR2, leading to increased IL-12 production, CD86 expression, and antigen uptake in immature DCs.
- DDR2 depletion significantly reduced IL-12 and CD86 upregulation in ColI-treated DCs.
- DDR2-ColI interaction enhances the capacity of mature DCs to activate allogeneic T cells.
Conclusions:
- DDR2 acts as a critical collagen receptor mediating DC activation.
- The DDR2-collagen interaction is vital for DC functional capacity and immune response regulation.
Related Concept Videos
T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
TGF - β Signaling Pathway
Inflammatory Bowel Disease III: Crohn's Disease
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
B Cell Activation and Differentiation
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

