Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Fricke, Ingo; Gabrilovich, Dmitry I.

doi:10.1080/08820130600803429

Cited by 145 publications

(118 citation statements)

References 168 publications

(150 reference statements)

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“…Our results further support other previous findings indicating that an increased VEGF is correlated with the reduced number of DCs in tumor tissue and in the peripheral blood of patients with various types of cancer (10,19). VEGF is known to promote tumor growth and inhibit the activation of nuclear factor κB (NF-κB) in endothelial progenitor cells, thereby inhibiting endothelial progenitor cells from differentiating into mature DCs (20). We speculated that VEGF released by Tca8113 cells induce monocytes differentiating into endothelial cells but not mature DCs.…”

Section: Discussionsupporting

confidence: 81%

Effect of siRNA-mediated downregulation of VEGF in Tca8113 cells on the activity of monocyte-derived dendritic cells

Wang

Huang

et al. 2012

Oncol Lett

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Section: Discussionsupporting

confidence: 81%

Effect of siRNA-mediated downregulation of VEGF in Tca8113 cells on the activity of monocyte-derived dendritic cells

Wang

Huang

et al. 2012

Oncol Lett

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“…Tumor-induced defects in the host immune system are currently believed to be critical in hindering tumor-specific immune responses, thereby limiting the benefits of cancer immunotherapy (26). A recent study by Mirza et al (20) reports the successful use of ATRA in reducing the numbers of immature myeloid suppressor cells in cancer patients, the accumulation of such cells being a major tumor escape mechanism, as well as improving DC function.…”

Section: Atra Enhances DC Migration Both In Vitro and In Vivomentioning

confidence: 99%

All-trans Retinoic Acid Enhances Murine Dendritic Cell Migration to Draining Lymph Nodes via the Balance of Matrix Metalloproteinases and Their Inhibitors

Darmanin

Chen²,

Zhao

et al. 2007

The Journal of Immunology

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Cancers escape immune surveillance through the manipulation of the host’s immune system. Sequestration of dendritic cells (DCs) within tumor tissues and the subsequent inhibition of their migration is one of the several mechanisms by which tumors induce immunosuppression. In view of recent findings depicting the improvement of tumor immune responses in cancer patients following all-trans retinoic acid (ATRA) treatment, we sought to identify the effects of ATRA on DC mobility in the context of tumor immunotherapy. Our results demonstrate that ATRA, added to differentiating murine bone marrow progenitor cells, enhances the invasive capacity of the resulting DCs. Immature DCs injected intratumorally in mice show increased accumulation in draining lymph nodes, but not in nondraining lymph nodes and spleens, when differentiated in the presence of ATRA. The in vitro migration of mature DCs through the basement membrane matrix toward the lymphoid chemokines CCL19 and CCL21 is enhanced in these cells, albeit not in the presence of a matrix metalloproteinase (MMP) inhibitor. An increase in MMP production with a simultaneous decrease in the production of their inhibitors (tissue inhibitors of matrix metalloproteinase or TIMPs) is provoked by ATRA. This affects the MMP/TIMP balance in DCs, in particular that of MMP-9 and TIMP-1, favoring protease activity and thus allowing for enhanced DC mobilization. In conclusion, this study demonstrates that ATRA is capable of improving DC trafficking in a tumor milieu and, in view of the encouraging results obtained in the clinic, further supports the notion that ATRA might be a valuable chemical adjuvant to current immunotherapeutic strategies for cancer.

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“…DCs are one of the most effective professional APCs. One of the many contributors that impede DC function in tumor defense is the buildup of ROS, which are present abundantly in the tumor microenvironment (Fricke and Gabrilovich 2006). High levels of ROS have been shown to induce oxidative stress, resulting in JNK-mediated denditric cell death (Handley et al 2005).…”

Section: Autophagy and Tumor Immunitymentioning

confidence: 99%

Autophagy and Cancer

Mah

Ryan

2011

Cold Spring Harbor Perspectives in Biology

147

109

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(Macro)autophagy is a cellular membrane trafficking process that serves to deliver cytoplasmic constituents to lysosomes for degradation. At basal levels, it is critical for maintaining cytoplasmic as well as genomic integrity and is therefore key to maintaining cellular homeostasis. Autophagy is also highly adaptable and can be modified to digest specific cargoes to bring about selective effects in response to numerous forms of intracellular and extracellular stress. It is not a surprise, therefore, that autophagy has a fundamental role in cancer and that perturbations in autophagy can contribute to malignant disease. We review here the roles of autophagy in various aspects of tumor suppression including the response of cells to nutrient and hypoxic stress, the control of programmed cell death, and the connection to tumor-associated immune responses.

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Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Cited by 145 publications

References 168 publications

Effect of siRNA-mediated downregulation of VEGF in Tca8113 cells on the activity of monocyte-derived dendritic cells

Effect of siRNA-mediated downregulation of VEGF in Tca8113 cells on the activity of monocyte-derived dendritic cells

All-trans Retinoic Acid Enhances Murine Dendritic Cell Migration to Draining Lymph Nodes via the Balance of Matrix Metalloproteinases and Their Inhibitors

Autophagy and Cancer

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