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Related Experiment Video

Updated: Sep 8, 2025

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Human Stem Cell-Derived β-cells Expressing An Optimized CD155 Reduce Cytotoxic Immune Cell Function for Application

Matthew E Brown1,2, Jessie M Barra1,3, Marcus R Pina1,2

  • 1Diabetes Institute, University of Florida, Gainesville, FL, USA.

Biorxiv : the Preprint Server for Biology
|August 20, 2025
PubMed
Summary

Engineered stem cell-derived beta cells (sBC) with high-affinity CD155 reduce immune attack, offering a promising new therapy for type 1 diabetes (T1D). This approach enhances immune evasion, improving sBC survival for potential restorative treatments.

Keywords:
CD155TIGITType 1 diabetesautoimmunitystem cell-derived β-like cell

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Area of Science:

  • Immunology
  • Stem Cell Biology
  • Endocrinology

Background:

  • Type 1 diabetes (T1D) treatment faces challenges with donor shortages and immune rejection of beta-cell replacement therapies.
  • Stem cell-derived beta-cells (sBC) offer a renewable source but are vulnerable to immune destruction.

Purpose of the Study:

  • To engineer human pluripotent stem cells to express a high-affinity mutant (Mut) variant of the immune checkpoint inhibitor CD155.
  • To evaluate the ability of modified sBC to evade immune attack mediated by T cells and NK cells.

Main Methods:

  • Human pluripotent stem cells were engineered to express wildtype (WT) or high-affinity mutant (Mut) CD155.
  • Modified cells were differentiated into sBC, and their immune interaction was assessed via co-culture studies.
  • The role of CD155-TIGIT signaling in immune evasion was confirmed using TIGIT blockade.

Main Results:

  • CD155 Mut-expressing sBC demonstrated upregulated CD155 and enhanced ligand binding.
  • CD155 Mut sBC suppressed CD8+ T cell and NK cell activation and proliferation by engaging TIGIT.
  • sBC expressing CD155 Mut showed reduced destruction by autoreactive immune cells and lower cytotoxic molecule secretion.

Conclusions:

  • High-affinity CD155 expression enhances immune evasion of sBC by utilizing the CD155-TIGIT inhibitory pathway.
  • This engineered immune evasion mechanism improves the therapeutic potential of sBC for type 1 diabetes.
  • Targeting CD155-TIGIT signaling represents a novel strategy for protecting beta-cell therapies from immune attack.