The ABC of dendritic cell development and function

Ven, Rieneke van de; Scheffer, George L.; Scheper, Rik J.; Gruijl, Tanja D. de

doi:10.1016/j.it.2009.06.004

Cited by 39 publications

(26 citation statements)

References 80 publications

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“…Similar with our observation, P-glycoprotein (Pgp; ABCB1), a molecule well known for its ability to transport of a broad spectrum of xenobiotics out of cells and thereby induce drug resistance, have important functions in DCs as blockade of ABCB1 inhibits differentiation, maturation and T cell-activating ability of MDDCs [20], [29], [31]. Although it has been shown that ABCG2 is required for MDDC and LC differentiation and migration [18], [32], [33], the inhibition of ABCG2 does not affect in DC maturation [18]. However, our results seem to be in disagreement with those of DC maturation results.…”

Section: Discussionsupporting

confidence: 81%

Inhibition of Breast Cancer Resistance Protein (ABCG2) in Human Myeloid Dendritic Cells Induces Potent Tolerogenic Functions during LPS Stimulation

et al. 2014

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Breast cancer resistance protein (ABCG2), a member of the ATP-binding cassette transporters has been identified as a major determinant of multidrug resistance (MDR) in cancer cells, but ABC transporter inhibition has limited therapeutic value in vivo. In this research, we demonstrated that inhibition of efflux transporters ABCG2 induced the generation of tolerogenic DCs from human peripheral blood myeloid DCs (mDCs). ABCG2 expression was present in mDCs and was further increased by LPS stimulation. Treatment of CD1c+ mDCs with an ABCG2 inhibitor, Ko143, during LPS stimulation caused increased production of IL-10 and decreased production of pro-inflammatory cytokines and decreased expression of CD83 and CD86. Moreover, inhibition of ABCG2 in monocyte-derived DCs (MDDCs) abrogated the up-regulation of co-stimulatory molecules and production of pro-inflammatory cytokines in these cells in response to LPS. Furthermore, CD1c+ mDCs stimulated with LPS plus Ko143 inhibited the proliferation of allogeneic and superantigen-specific syngenic CD4+ T cells and promoted expansion of CD25+FOXP3+ regulatory T (Treg) cells in an IL-10-dependent fashion. These tolerogenic effects of ABCG2 inhibition could be abolished by ERK inhibition. Thus, we demonstrated that inhibition of ABCG2 in LPS-stimulated mDCs can potently induce tolerogenic potentials in these cells, providing crucial new information that could lead to development of better strategies to combat MDR cancer.

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Section: Discussionsupporting

confidence: 81%

Inhibition of Breast Cancer Resistance Protein (ABCG2) in Human Myeloid Dendritic Cells Induces Potent Tolerogenic Functions during LPS Stimulation

et al. 2014

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“…The clustering of dendritic cells with each other is known to occur in a number of autoimmune diseases. [9][10][11][12] It is tempting, therefore, to speculate that the presence of aggregates of dendritic cells observed in esophageal tissues might represent an ongoing autoimmune reaction or that autoimmune mechanisms are at least involved. The issue of whether the clustering of dendritic cells might relate to the reduced levels of C1q expression in Barrett's esophagus and esophageal adenocarcinoma requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7] We recently reported that antigen-presenting dendritic cells are present in Barrett's esophagus, with a significant increase in their spatial density in adenocarcinoma compared to benign Barrett's esophagus. 8 Because dendritic cells are powerful initiators and regulators of immune reactions, [9][10][11] we hypothesized that dendritic cells may play a role in the pathogenesis of Barrett's esophagus and adenocarcinoma. 8 In that study 8 we noted the formation of focal aggregations of dendritic cells as well as the occurrence of dendritic cells and T cells contacting each other in Barrett's esophagus and adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

Bobryshev

Lord

2010

Journal of Gastrointestinal Surgery

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“…Finally, many signaling lipids with established roles in tumor biology are substrates of ABC transporters and their enhanced efflux can result in enhanced activation of various signaling pathways. 53,68 To summarize, the main limitations of ABC-inhibitors are: (i) toxicities due to elevated doses needed to observe a pharmacological effect; (ii) PK interactions with anticancer drugs; (iii) lack of specificity; (iv) impaired anti-tumor immune response and (v) their pluripotent action on various processes involved in cancer progression without sufficient knowledge of the causal connection between this progression and the ABC transporter expression.…”

Section: Increased Drug Effluxmentioning

confidence: 99%

How can nanomedicines overcome cellular-based anticancer drug resistance?

2016

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Despite the great progress in the field of cancer research, complete remission of cancer patients is a rarely seen outcome in clinics. The failure of a plethora of promising anticancer drugs is mostly due to the insurgence of multidrug resistance (MDR) phenomena with various factors, both physio-pathological and cellular, being responsible for their development. Over the past 40 years, the impressive progress in the nanotechnology field and its application in medicine (i.e., nanomedicine) enabled the development of novel cancer treatments with improved specificity and efficacy, mainly referring to the possibility to overcome MDR. However, the emergence of many nanomedicines defined in the literature as ''overcoming the resistance'' has resulted in very few of them eventually being approved for clinical application and reaching the marketplace (liposomal formulation of doxorubicin (Myocet s , Caelix s ) and paclitaxel nanoparticles (Abraxane s ), for instance). The capacity of nanomedicines to overcome physio-pathologicalbased resistance by enhancing drug accumulation at the tumor site via passive and ligand-mediated targeting has been largely reviewed in the past few years. This review will specifically focus on the cellular mechanisms involved in the MDR, which will be discussed with respect to the cellular site in which their action is exerted (that is, membrane, cytoplasm or nucleus). A complete overview of various nanomedicines designed to bypass or directly inhibit each of these specific resistance mechanisms will be offered.

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The ABC of dendritic cell development and function

Cited by 39 publications

References 80 publications

Inhibition of Breast Cancer Resistance Protein (ABCG2) in Human Myeloid Dendritic Cells Induces Potent Tolerogenic Functions during LPS Stimulation

Inhibition of Breast Cancer Resistance Protein (ABCG2) in Human Myeloid Dendritic Cells Induces Potent Tolerogenic Functions during LPS Stimulation

Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

How can nanomedicines overcome cellular-based anticancer drug resistance?

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