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Human stem cell-derived β cells expressing an optimized CD155 reduce cytotoxic immune cell function for application

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Engineered stem cell-derived beta cells (sBC) express high-affinity CD155 to evade immune attack. This approach enhances sBC survival, offering a promising new therapy for type 1 diabetes (T1D).

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Area of Science:

  • Immunology
  • Endocrinology
  • Regenerative Medicine

Background:

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

Purpose of the Study:

  • To engineer human pluripotent stem cells for enhanced immune evasion of sBC.
  • To investigate the role of CD155-TIGIT signaling in protecting sBC from immune destruction.

Main Methods:

  • Human pluripotent stem cells were engineered to express wild-type or high-affinity mutant CD155.
  • Engineered cells were differentiated into sBC and co-cultured with immune cells.
  • Immune cell activation, sBC destruction, and cytotoxic molecule secretion were assessed, with and without TIGIT blockade.

Main Results:

  • CD155-expressing sBC suppressed autoreactive CD8+ T cell and NK cell activation.
  • Engaging the TIGIT receptor mediated this suppression, reducing immune cell-mediated sBC destruction.
  • TIGIT blockade abolished the protective effect, confirming the CD155-TIGIT pathway's role.

Conclusions:

  • High-affinity CD155 expression enhances sBC immune evasion.
  • This strategy improves sBC survival and holds potential for T1D cell replacement therapy.