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February 7, 2026Stem Cell Research & TherapyOpen Access

PTPN2 deficiency amplifies inflammatory signalling and impairs functional maturation of human stem cell-derived islets

Valerie Vandenbempt Javier Negueruela Francisco Ribeiro-Costa Mariana Nunes Leonardo Traini Sema Elif Eski Wadsen St-Pierre-Wijckmans Stéphane Demine Nicolas Baeyens Hazem Ibrahim Luciano G. Martelotto Sumeet Pal Singh Alessandra K. Cardozo Mayank Bansal Esteban N. Gurzov

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Key Points

This research examines the role of PTPN2 in maintaining β-cell function under inflammation and metabolic stress.
Analyzed PTPN2 deficiency in human stem cell-derived islets (SC-islets)
Assessed inflammatory signalling pathways
Evaluated functional maturation of β-cells
PTPN2 deficiency led to increased inflammatory signalling
Functional maturation of β-cells was impaired
Identified critical roles of PTPN2 during metabolic stress

Implication

Research demonstrates impaired β-cell function due to PTPN2 deficiency in stem cell-derived islets, indicating critical roles in inflammation.

Abstract

Our study postulates a key role of PTPN2 in preserving β-cell function during inflammatory and metabolic stress in SC-islets.

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Cite This Study

Vandenbempt et al. (2026) studied this question.

synapsesocial.com/papers/698acaad7c832249c30b9fed https://doi.org/10.1186/s13287-025-04892-4

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Keep reading

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Myeloid-Intrinsic Protein Tyrosine Phosphatase Non-Receptor Type 2 (PTPN2) Programs Hematopoietic Stem Cells Towards Pro-Inflammatory Macrophages 2309892Original Research · 2026
2PTPN2 sustains non-canonical inflammasome activation and shapes the inflammatory response to sepsisOriginal Research · 2026
3PTPN2 alleviates psoriasis by targeting the STING-STAT3 axis and restoring autophagy: in vitro and in vivo evidenceOriginal Research · 2026 · 2 citations
4Molecular Mechanisms and Targeted Therapies of PTPN2 in Metabolic Diseases: A ReviewReview · 2026
5PTPN22 mediates delayed negative feedback of T cell activation by forming an inhibitory signaling complexOriginal Research · 2026

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