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Updated: Apr 25, 2026

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
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Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells

Published on: August 1, 2025

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DYRK1A enhances antitumor immunity in type 1 conventional dendritic cells via mTORC1 activation

Hongjiao Wang1, He Jiang1, Songlin He2

  • 1State Key Laboratory of Cellular Stress Biology, Department of Oncology, Xiang'an Hospital of Xiamen University, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, Fujian, China.

The Journal of Clinical Investigation
|April 23, 2026
PubMed

Insights

Dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) is crucial for type 1 conventional dendritic cell (cDC1) function. This kinase regulates antitumor immunity by controlling Tsc2 degradation and mTORC1 signaling, offering cancer immunotherapy targets.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cancer Research

Background:

  • Type 1 conventional dendritic cells (cDC1s) are vital for immune responses and homeostasis.
  • The precise molecular mechanisms governing cDC1 functions are not fully understood.

Purpose of the Study:

  • To identify key regulators of cDC1 function.
  • To elucidate the molecular mechanisms by which these regulators impact antitumor immunity.

Main Methods:

  • Genetic ablation of Dyrk1a in cDC1s in murine models.
  • Analysis of DYRK1A-mediated phosphorylation of TSC2.
  • Assessment of mTORC1 signaling pathway activation.
  • Evaluation of antitumor immune responses and tumor progression.
  • Correlation analysis with effector T-cell responses in human cancers.

Main Results:

  • DYRK1A was identified as a critical kinase regulating cDC1 function upon stimulation.
  • Genetic deletion of Dyrk1a in cDC1s impaired antitumor immunity and accelerated tumor growth.
  • DYRK1A promotes mTORC1 signaling in cDC1s by phosphorylating and degrading TSC2.
  • Restoring Tsc2 in Dyrk1a-deficient cDC1s rescued antitumor functions.
  • DYRK1A-mTORC1 signaling in cDC1s positively correlates with T-cell responses in human cancers.

Conclusions:

  • The DYRK1A-TSC2-mTORC1 signaling axis is essential for cDC1-mediated antitumor immunity.
  • Targeting this pathway presents a potential strategy for enhancing cancer immunotherapy.
Keywords:
Cell biologyDendritic cellsImmunology

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