ArticleFrontiers in immunology2025
Sepsis prevents the development of experimental type 1 diabetes.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Peripheral Blood Mononuclear Cells in Sepsis: Immune Trajectories, Monocyte Dysfunction, and Translational Biomarkers.Journal of inflammation research · 2026Review
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Authors and funding
8 authors.
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Abstract
Introduction: While both sepsis and autoimmunity are characterized by dysregulated immune responses, their mutual influence remains only partially understood. Methods: In this study, we investigated how sepsis affects the development of type 1 diabetes (T1D), an autoimmune disease characterized by the destruction of pancreatic β-cells. Specifically, we examined the impact of polymicrobial sepsis on the progression of T1D induced by multiple low doses of streptozotocin (MLDS). C57BL/6 mice were subjected to cecal ligation and puncture (CLP) to induce sepsis, and T1D was subsequently induced using the MLDS protocol after the mice had fully recovered from the acute phase of sepsis. Results and discussion: Although CLP triggered transient hypoglycemia, it did not impair the structure or function of the endocrine pancreas, and the mice were normoglycemic at the time of T1D induction. Notably, CLP limited immune cell infiltration into the pancreas following MLDS treatment, thereby preventing the onset of T1D and the development of hyperglycemia. CD4
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