ArticleDiabetologia2026
Characterisation of human pancreatic mesenchymal stromal cells in type 1 diabetes.
Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
aims/hypothesisCulture-expanded mesenchymal stromal cells (MSCs) reduce immune cell activation and improve islet functional survival. However, little is known about human pancreatic MSCs (pMSCs) in health or how they are altered in type 1 diabetes. Here, we determined the number, density and islet-protective phenotype of pMSCs in situ in individuals with and without type 1 diabetes.
methodsMultiplex immunohistochemistry was used to identify pMSCs (CD90
resultspMSCs were identified in situ in the human pancreas where they wrap around the islet periphery in an expected spindle-like morphology. ANXA1 was expressed by 33.2% of pMSCs and was expressed constitutively among individuals with or without diabetes. The density of both intraislet pMSCs and pMSCs within 10 µm of the islet periphery was increased for insulin-containing islets in individuals with type 1 diabetes compared with individuals without diabetes (p<0.001). pMSC density within 10 µm of the islet periphery was preferentially increased in individuals ≥13 years at type 1 diabetes diagnosis compared with individuals <13 years at type 1 diabetes diagnosis (p<0.001). pMSC density was reduced around insulin-deficient islets compared with insulin-containing islets in individuals with diabetes (p<0.001), consistent with an islet-protective role for pMSCs. Exposure of culture-expanded MSCs to an aggressive cytokine combination led to increased cell death and reduced proliferation. CONCLUSIONS/
interpretationpMSCs express ANXA1 constitutively, suggesting an islet-protective role in health. The density of pMSCs was increased around insulin-containing islets and lost around insulin-deficient islets in individuals with type 1 diabetes which aligns with this hypothesis. pMSC density at the periphery of insulin-containing islets was preferentially higher in individuals with later-onset type 1 diabetes, correlating with a less intense immune cell infiltration. The reduced ability of pMSCs to survive in the more intense proinflammatory environment around islets in younger-onset type 1 diabetes may contribute to the rapid rate of beta cell loss in these individuals.
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