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Assessing the Development of Murine Plasmacytoid Dendritic Cells in Peyer's Patches Using Adoptive Transfer of Hematopoietic Progenitors
Published on: March 17, 2014
Stromal-derived factor-1 in human tumors recruits and alters the function of plasmacytoid precursor dendritic cells
W Zou1, V Machelon, A Coulomb-L'Hermin
1Tulane Medical School, Section of Hematology and Medical Oncology, New Orleans, Louisiana, USA. wzou@tulane.edu
Abstract:
Dendritic-cell (DC) trafficking and function in tumors is poorly characterized, with studies confined to myeloid DCs (DC1s). Tumors inhibit DC1 migration and function, likely hindering specific immunity. The role of plasmacytoid DCs (DC2s) in tumor immunity is unknown. We show here that malignant human ovarian epithelial tumor cells express very high levels of stromal-derived factor-1, which induces DC2 precursor (preDC2) chemotaxis and adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC2s from tumor macrophage interleukin-10-induced apoptosis, all through CXC chemokine receptor-4. The VLA-5 ligand vascular-cell adhesion molecule-1 mediated preDC2 adhesion/transmigration. Tumor preDC2s induced significant T-cell interleukin-10 unrelated to preDC2 differentiation or activation state, and this contributed to poor T-cell activation. Myeloid precursor DCs (preDC1s) were not detected. Tumors may weaken immunity by attracting preDC2s and protecting them from the harsh microenvironment, and by altering preDC1 distribution.
Insights
Ovarian tumors attract plasmacytoid dendritic cells (DC2s) via stromal-derived factor-1, promoting tumor growth. These tumor-infiltrating DC2s suppress T-cell immunity, potentially weakening the anti-tumor response.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Dendritic cell (DC) roles in tumor immunity are incompletely understood, particularly plasmacytoid DCs (DC2s).
- Myeloid DCs (DC1s) are known to be inhibited by tumors, potentially impairing anti-tumor responses.
Purpose of the Study:
- To investigate the role of plasmacytoid dendritic cells (DC2s) in human ovarian epithelial tumors.
- To elucidate the mechanisms by which tumor cells influence DC2 precursor (preDC2) behavior and function within the tumor microenvironment.
Main Methods:
- Analysis of human ovarian epithelial tumor cells and associated immune cells.
- Assessment of preDC2 chemotaxis, adhesion, and transmigration in response to tumor-derived factors.
- Evaluation of preDC2 apoptosis regulation and T-cell cytokine production.
Main Results:
- Malignant ovarian tumor cells highly express stromal-derived factor-1 (SDF-1), which chemoattracts and promotes adhesion/transmigration of preDC2s via CXC chemokine receptor-4 (CXCR4).
- Tumor-derived SDF-1 upregulates very late antigen-5 (VLA-5) on preDC2s, facilitating adhesion via vascular cell adhesion molecule-1 (VCAM-1) and protecting them from IL-10-induced apoptosis.
- Tumor-recruited preDC2s induce IL-10 production in T-cells, contributing to impaired T-cell activation and potentially suppressing anti-tumor immunity.
Conclusions:
- Ovarian tumors actively recruit preDC2s and protect them within the tumor microenvironment, suggesting a mechanism for immune evasion.
- The interaction between tumor cells and preDC2s, mediated by SDF-1/CXCR4 and VLA-5/VCAM-1, leads to immunosuppression through T-cell IL-10 induction.
- Tumors may weaken host immunity by manipulating DC2 trafficking and function, alongside potential alterations in DC1 distribution.
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