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Naive T cells that have not yet encountered an antigen express two primary CD...
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DNGR-1 signalling limits dendritic cell activation for optimal antigen cross-presentation.

Michael D Buck1, Tomás Castro-Dopico2, Oliver Schulz2

  • 1Immunobiology Laboratory, The Francis Crick Institute, London, UK. michael.buck@crick.ac.uk.

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|October 30, 2025
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Summary

DNGR-1 receptor signaling in dendritic cells (DCs) prioritizes antigen cross-presentation over cell activation. This balance may minimize inflammation from dead cells, impacting immune responses to cancer and viruses.

Keywords:
ActivationCLEC9ACross-presentationDNGR-1cDC1

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Innate immune receptors on dendritic cells (DCs) typically drive immune responses.
  • DNGR-1 (CLEC9A) on type 1 conventional DCs (cDC1s) recognizes F-actin on dead cells, promoting antigen cross-presentation for anti-viral and anti-cancer immunity.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying DNGR-1 function in cDC1s.
  • To elucidate the role of a specific amino acid residue in DNGR-1 signaling and its impact on receptor activation and antigen cross-presentation.

Main Methods:

  • Site-directed mutagenesis of the DNGR-1 receptor.
  • In vitro assays to assess cDC1 activation.
  • Evaluation of antigen cross-presentation capacity.

Main Results:

  • A single amino acid substitution in DNGR-1 altered its signaling, converting it into an activating receptor but reducing antigen cross-presentation.
  • The reverse mutation in the related Dectin-1 receptor impaired activation while enhancing cross-presentation.
  • SHIP1 phosphatase recruitment, regulated by this residue, influences DNGR-1's functional output.

Conclusions:

  • DNGR-1 exhibits a functional trade-off, prioritizing antigen cross-presentation over cDC1 activation.
  • This evolved mechanism may serve to limit inflammatory responses to dead cells.
  • Findings provide insights into fine-tuning immune receptor signaling for specific biological outcomes.