ArticleImmunity & ageing : I & A2026
Toll-like receptor 2 modulates age-associated insulitis and fibrotic remodeling of Langerhans islets.
Article in Immunity & ageing : I & A, 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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Abstract
backgroundThe steadily increasing aging population highlights the importance of maintaining health at an advanced age. Metabolic diseases are among the most prevalent age-related disorders, and the Langerhans islets, critical regulators of glucose homeostasis, are particularly susceptible to disturbed insulin secretion and functional decline. Multiple stimuli contribute to islet dysfunction during aging, including bacterial products that increase with age and can activate Toll-like receptor (TLR) signaling. TLR2, which recognizes a broad spectrum of microbial ligands including components from Gram-positive bacteria, has been implicated in type 2 diabetes; however, its role in β-cell function during aging remains unclear. Accordingly, we hypothesize that TLR2 signaling contributes to inflammation and remodeling during aging in Langerhans islets.
resultsTo determine the role of TLR2 in islet aging, we compared young and old male TLR2-deficient mice with age-matched C57BL/6J controls. Old TLR2
conclusionsOverall, our results suggest that TLR2 signaling contributes to immune cell accumulation and fibrotic remodeling during aging, linking inflammation to pancreatic islet aging in mice. These findings identify TLR2 as a potential mediator of age-related islet dysfunction and a candidate target for further investigation.
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