Skip to content
DraconiticResearch
Search Sources API
201,683 studies31 sourcesUpdated 31 min ago
Peer-reviewedCC BY 4.0Frontiers in Immunology

Dendritic cell fate plasticity: a central switch in the tumor immune landscape

Abstract

Dendritic cells (DCs) are key antigen-presenting cells that initiate antitumor immunity, yet DCs in the tumor microenvironment (TME) are often functionally impaired. Unlike previous reviews that focus on DC dysfunction, this review argues that the main effect of the TME on DCs is not passive dysfunction but active fate hijacking. Through this hijacking, DC populations and states are shifted from antitumor sentinels toward immunosuppressive accomplices. This review follows a causal chain from fate determination, through fate deviation, to fate reprogramming. It first describes how the lineage fate of DC subsets is determined by transcription factor networks. It then summarizes how the TME hijacks DC fate through hierarchical mechanisms, including metabolic deprivation, inhibitory signals, epigenetic remodeling, death evasion, and physical barriers. Two reprogramming strategies are discussed: direct DC modification and indirect niche remodeling. Finally, the review focuses on precision interventions that depend on tumor type and niche. This review systematically covers 129 publications from 2008 to 2026, including 90 original studies, 8 clinical studies, and 31 reviews. Together, this synthesis provides an actionable framework for DC-centered precision immunotherapy.

Related

  1. An endocannabinoid-nitric oxide signaling switch triggers reciprocal inhibitory-excitatory plasticity at dopamine neuron inputs following prenatal cannabinoid exposure
    V. Serra, F. Brandalise, V. Miczan +2
    bioRxivPreprintAll rights reservedFull textNeurosciencebioRxiv
  2. Integrative analysis of the MDM2 promoter switch and cellular lineage plasticity in colorectal cancer: a contrast between the autonomous-proliferation type (CIN/CMS2) and the environment-adaptive type (MSI/gastric metaplasia)
    T. Tsukui, K. Tsuda, R. Yao +1
    bioRxivPreprintCC BYFull textBioinformatics & computational biologybioRxiv
  3. Uncovering a cryptic allosteric hub governing energy landscape plasticity within the Nur77 ligand-binding domain
    Lang Chen, Jiawen Chen, Conggang Li +2
    Magnetic Resonance LettersPeer-reviewedCC BY-NC-NDFull textNeuroscienceDOAJEurope PMCEurope PMCPMC
  4. Targeting Dendritic Cells in Cancer Immunotherapy: From Immune Priming to Tumor Microenvironment Reprogramming
    Serena Zanotta, Domenico Galati
    International Journal of Molecular SciencesPeer-reviewedCC BY 4.0ImmunologyCrossref
  5. Stochastic gradient descent on the epigenetic landscape: a unified framework for cellular plasticity, tumor heterogeneity, and the asymptotic irrelevance of fitness
    Artur C. Fassoni
    arXivPreprintarXiv licenceFull textCell biologyEvolutionary biologyarXiv
BibTeX
@article{lu2026dendritic,
  title = {{Dendritic cell fate plasticity: a central switch in the tumor immune landscape}},
  author = {Jianing Lu and Yan Zhuang and Dongwei Yao and Wei Hu and Feng Lu},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = nov,
  doi = {10.3389/fimmu.2026.2010764},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.2010764},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Dendritic cell fate plasticity: a central switch in the tumor immune landscape
AU  - Jianing Lu
AU  - Yan Zhuang
AU  - Dongwei Yao
AU  - Wei Hu
AU  - Feng Lu
PY  - 2026
DA  - 2026/11/04
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.2010764
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.2010764
AB  - Dendritic cells (DCs) are key antigen-presenting cells that initiate antitumor immunity, yet DCs in the tumor microenvironment (TME) are often functionally impaired. Unlike previous reviews that focus on DC dysfunction, this review argues that the main effect of the TME on DCs is not passive dysfunction but active fate hijacking. Through this hijacking, DC populations and states are shifted from antitumor sentinels toward immunosuppressive accomplices. This review follows a causal chain from fate determination, through fate deviation, to fate reprogramming. It first describes how the lineage fate of DC subsets is determined by transcription factor networks. It then summarizes how the TME hijacks DC fate through hierarchical mechanisms, including metabolic deprivation, inhibitory signals, epigenetic remodeling, death evasion, and physical barriers. Two reprogramming strategies are discussed: direct DC modification and indirect niche remodeling. Finally, the review focuses on precision interventions that depend on tumor type and niche. This review systematically covers 129 publications from 2008 to 2026, including 90 original studies, 8 clinical studies, and 31 reviews. Together, this synthesis provides an actionable framework for DC-centered precision immunotherapy.
SN  - 1664-3224
ER  -