Vaccines Targeting Dendritic Cells

A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Cancer Vaccines and Immunotherapy".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 1317

Special Issue Editors


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Guest Editor
Luminex Corporation – A DiaSorin Company, Austin, TX 78727, USA
Interests: dendritic cell (subsets); cytotoxic T cells; viral infections; cancer; biomarkers

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Guest Editor
Institute for Molecular Medicine, Paul Klein Center for Immune Intervention, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany
Interests: Langerhans cells; dendritic cells (subsets); immune regulation; inflammation; cancer

Special Issue Information

Dear Colleagues,

Dendritic cells (DCs) act as the sentinels of the immune system and initiate and orchestrate immune responses. Current DC-based immunotherapy approaches have shown promise in cancer treatment and prevention. These approaches involve the activation of DCs following the in vitro and in vivo delivery of antigens directly to them using specialized systems such as nanoparticles or viral vectors. These strategies aim to induce humoral immunity, prime T helper cells, and/or elicit CTL responses. Broadly, the role of DCs in modulating adaptive immune responses offers new avenues for vaccine development.

This Special Issue aims to compile the latest research on the ongoing advancements in vaccines targeting DCs. We welcome the submission of reviews, research articles, and short communications that highlight recent breakthroughs in DC-targeting vaccines, as well as manuscripts addressing the challenges and limitations encountered in this field.

Dr. Ronald A. Backer
Prof. Dr. Björn E. Clausen
Guest Editors

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Keywords

  • vaccines
  • dendritic cells
  • antigen targeting
  • immune responses
  • adjuvant
  • cancer immunotherapy
  • T cell activation

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Published Papers (1 paper)

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Research

19 pages, 6886 KiB  
Article
GSK-3β in Dendritic Cells Exerts Opposite Functions in Regulating Cross-Priming and Memory CD8 T Cell Responses Independent of β-Catenin
by Chunmei Fu, Jie Wang, Tianle Ma, Congcong Yin, Li Zhou, Björn E. Clausen, Qing-Sheng Mi and Aimin Jiang
Vaccines 2024, 12(9), 1037; https://doi.org/10.3390/vaccines12091037 - 10 Sep 2024
Viewed by 989
Abstract
GSK-3β plays a critical role in regulating the Wnt/β-catenin signaling pathway, and manipulating GSK-3β in dendritic cells (DCs) has been shown to improve the antitumor efficacy of DC vaccines. Since the inhibition of GSK-3β leads to the activation of β-catenin, we hypothesize that [...] Read more.
GSK-3β plays a critical role in regulating the Wnt/β-catenin signaling pathway, and manipulating GSK-3β in dendritic cells (DCs) has been shown to improve the antitumor efficacy of DC vaccines. Since the inhibition of GSK-3β leads to the activation of β-catenin, we hypothesize that blocking GSK-3β in DCs negatively regulates DC-mediated CD8 T cell immunity and antitumor immunity. Using CD11c-GSK-3β−/− conditional knockout mice in which GSK-3β is genetically deleted in CD11c-expressing DCs, we surprisingly found that the deletion of GSK-3β in DCs resulted in increased antitumor immunity, which contradicted our initial expectation of reduced antitumor immunity due to the presumed upregulation of β-catenin in DCs. Indeed, we found by both Western blot and flow cytometry that the deletion of GSK-3β in DCs did not lead to augmented expression of β-catenin protein, suggesting that GSK-3β exerts its function independent of β-catenin. Supporting this notion, our single-cell RNA sequencing (scRNA-seq) analysis revealed that GSK-3β-deficient DCs exhibited distinct gene expression patterns with minimally overlapping differentially expressed genes (DEGs) compared to DCs with activated β-catenin. This suggests that the deletion of GSK-3β in DCs is unlikely to lead to upregulation of β-catenin at the transcriptional level. Consistent with enhanced antitumor immunity, we also found that CD11c-GSK-3β−/− mice exhibited significantly augmented cross-priming of antigen-specific CD8 T cells following DC-targeted vaccines. We further found that the deletion of GSK-3β in DCs completely abrogated memory CD8 T cell responses, suggesting that GSK-3β in DCs also plays a negative role in regulating the differentiation and/or maintenance of memory CD8 T cells. scRNA-seq analysis further revealed that although the deletion of GSK-3β in DCs positively regulated transcriptional programs for effector differentiation and function of primed antigen-specific CD8 T cells in CD11c-GSK-3β−/− mice during the priming phase, it resulted in significantly reduced antigen-specific memory CD8 T cells, consistent with diminished memory responses. Taken together, our data demonstrate that GSK-3β in DCs has opposite functions in regulating cross-priming and memory CD8 T cell responses, and GSK-3β exerts its functions independent of its regulation of β-catenin. These novel insights suggest that targeting GSK-3β in cancer immunotherapies must consider its dual role in CD8 T cell responses. Full article
(This article belongs to the Special Issue Vaccines Targeting Dendritic Cells)
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