Abstract

Dendritic cells (DCs) are efficient antigen-presenting cells (APCs) and potent activators of naïve T cells. Therefore, they act as a connective ring between innate and adaptive immunity. DC subsets are heterogeneous in their ontogeny and functions. They have proven to potentially take up and process tumor-associated antigens (TAAs). In this regard, researchers have developed strategies such as genetically engineered or TAA-pulsed DC vaccines; these manipulated DCs have shown significant outcomes in clinical and preclinical models. Here, we review DC classification and address how DCs are skewed into an immunosuppressive phenotype in cancer patients. Additionally, we present the advancements in DCs as a platform for cancer immunotherapy, emphasizing the technologies used for in vivo targeting of endogenous DCs, ex vivo generated vaccines from peripheral blood monocytes, and induced pluripotent stem cell-derived DCs (iPSC-DCs) to boost antitumoral immunity.

Highlights

  • Cancer evades immune surveillance as one of its hallmarks and prevents the immune system from tumor eradication (Hanahan and Weinberg, 2011; Mittal et al, 2014)

  • GVAX is one of the first tested vaccines against pancreatic cancer, and it is composed of the dendritic cells (DCs) Vaccines in Cancer Immunotherapy irradiated tumor cell-expressing granulocyte-macrophage colony-stimulating factor (GM-CSF) (Le et al, 2015; Yarchoan et al, 2020)

  • This review provides a brief overview of the main DC subsets and illustrates how DC and cancer cell crosstalk in the tumor microenvironment (TME) correlates with a positive or negative prognosis

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Summary

Introduction

Cancer evades immune surveillance as one of its hallmarks and prevents the immune system from tumor eradication (Hanahan and Weinberg, 2011; Mittal et al, 2014). In clinical and preclinical melanoma models, different strategies of antigen delivery or loading onto pDCs resulted in significant type I IFN production, antigenspecific T-cell priming, and superior chemoattractive properties to cDC2s, eliciting antitumor activity (Tel et al, 2013; Kranz et al, 2016; van Beek et al, 2020).

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