JNK activation limits dendritic cell maturation in response to reactive oxygen species by the induction of apoptosis

Handley, Matthew E.; Thakker, Manish; Pollara, Gabriele; Chain, Benjamin M.; Katz, David R.

doi:10.1016/j.freeradbiomed.2005.02.022

Cited by 36 publications

(33 citation statements)

References 58 publications

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“…Moreover, this study showed that limiting ROS loads is a major NF-κB function that results in the control of JNK activity in DCs. A current study showed that hydrogen peroxide, at low concentrations, activated p38 but did not alter DC phenotype (Handley, et al 2005). However, increased concentrations of hydrogen peroxide activated both p38 and JNK, leading to inhibition of tyrosine phosphatases by JNK in DC and induction of apoptosis.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 48%

“…However, increased concentrations of hydrogen peroxide activated both p38 and JNK, leading to inhibition of tyrosine phosphatases by JNK in DC and induction of apoptosis. JNK inhibitors partially protected the DC from the proapoptotic effects, whereas hydrogen peroxide and LPS synergized in inducing JNK activation and DC apoptosis (Handley, et al 2005).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 97%

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Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Fricke

Gabrilovich

2006

Immunological Investigations

145

112

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The fact that the immune response to cancer is compromised has been convincingly demonstrated in murine tumor models as well as in cancer patients. The unresponsiveness of the host immune system is one of the major mechanisms of tumor escape as well as an important factor that limits the success of cancer immunotherapy. Inadequate function of professional antigen presenting cells dendritic cells (DC) in cancer is one of the major elements of compromised anti-tumor immune response. Despite substantial progress in recent years, the mechanism of inadequate DC function in cancer still remains unclear. The tumor microenvironment has emerged as an important component contributing to DC malfunction. In this review we will discuss the potential role of tumor microenvironment in DC dysfunction.

show abstract

Section: Reactive Oxygen Speciesmentioning

confidence: 48%

Section: Reactive Oxygen Speciesmentioning

confidence: 97%

Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Fricke

Gabrilovich

2006

Immunological Investigations

145

112

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“…Suppression of p38 or extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation by inhibitors prevents DC maturation, whereas activation of c-Jun N-terminal kinase (JNK) may limit DC maturation (23)(24)(25). To determine whether DMF alters MAPK signaling (see Fig.…”

Section: Dmf Inhibits the Nf-b Pathway In Dcs-mentioning

confidence: 99%

Dimethyl Fumarate Inhibits Dendritic Cell Maturation via Nuclear Factor κB (NF-κB) and Extracellular Signal-regulated Kinase 1 and 2 (ERK1/2) and Mitogen Stress-activated Kinase 1 (MSK1) Signaling

Peng

Guerau-de-Arellano

Mehta

et al. 2012

Journal of Biological Chemistry

169

186

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“…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). Because autophagy has a major role in buffering ROS, a defect in this lysosomal degradation pathway would handicap DCs due to the accumulation of ROS.…”

Section: Autophagy and Tumor Immunitymentioning

confidence: 99%

Autophagy and Cancer

Mah

Ryan

2011

Cold Spring Harbor Perspectives in Biology

143

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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JNK activation limits dendritic cell maturation in response to reactive oxygen species by the induction of apoptosis

Cited by 36 publications

References 58 publications

Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Dendritic Cells and Tumor Microenvironment: A Dangerous Liaison

Dimethyl Fumarate Inhibits Dendritic Cell Maturation via Nuclear Factor κB (NF-κB) and Extracellular Signal-regulated Kinase 1 and 2 (ERK1/2) and Mitogen Stress-activated Kinase 1 (MSK1) Signaling

Autophagy and Cancer

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