| 1. |
- Galgani, Mario, et al.
(författare)
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Meta-Immunological Profiling of Children With Type 1 Diabetes Identifies New Biomarkers to Monitor Disease Progression
- 2013
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 62:7, s. 2481-2491
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Tidskriftsartikel (refereegranskat)abstract
- Type 1 diabetes is characterized by autoimmurte destruction of pancreatic beta-cells in genetically susceptible individuals. Triggers of islet autoimmunity, time course, and the precise mechanisms responsible for the progressive beta-cell failure are not completely understood. The recent escalation of obesity in affluent countries has been suggested to contribute to the increased incidence of type 1 diabetes. Understanding the link between metabolism and immune tolerance could lead to the identification of new markers for the monitoring of disease onset and progression. We studied several immune cell subsets and factors with high metabolic impact as markers associated with disease progression in high-risk subjects and type 1 diabetic patients at onset and at 12 and 24 months after diagnosis. A multiple correlation matrix among different parameters was evaluated statistically and assessed visually on two-dimensional graphs. Markers to predict residual beta-cell function up to 1 year after diagnosis were identified in multivariate logistic regression models. The meta-immunological profile changed significantly over time in patients, and a specific signature that was associated with worsening disease was identified. A multivariate logistic regression model measuring age, BMI, fasting C-peptide, number of circulating CD3(+)CD16(+)CD56(+) cells, and the percentage of CD1c(+)CD19(-)CD14(-)CD303(-) type 1 myeloid dendritic cells at disease onset had a significant predictive value. The identification of a specific meta-immunological profile associated with disease status may contribute to our understanding of the basis of diabetes progression.
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| 2. |
- Mantini, Cesare, et al.
(författare)
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A highly-detailed anatomical study of left atrial auricle as revealed by in-vivo computed tomography
- 2023
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Ingår i: Heliyon. - 2405-8440. ; 9:10
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Forskningsöversikt (refereegranskat)abstract
- The left atrial auricle (LAA) is the main source of intracardiac thrombi, which contribute significantly to the total number of stroke cases. It is also considered a major site of origin for atrial fibrillation in patients undergoing ablation procedures. The LAA is known to have a high degree of morphological variability, with shape and structure identified as important contributors to thrombus formation. A detailed understanding of LAA form, dimension, and function is crucial for radiologists, cardiologists, and cardiac surgeons. This review describes the normal anatomy of the LAA as visualized through multiple imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI), and echocardiography. Special emphasis is devoted to a discussion on how the morphological characteristics of the LAA are closely related to the likelihood of developing LAA thrombi, including insights into LAA embryology.
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| 3. |
- Terrazzano, Giuseppe, et al.
(författare)
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T1D progression is associated with loss of CD3+CD56+ regulatory T cells that control CD8+ T cell effector functions
- 2020
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Ingår i: Nature Metabolism. - : Springer Science and Business Media LLC. - 2522-5812. ; 2:2, s. 142-152
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Tidskriftsartikel (refereegranskat)abstract
- An unresolved issue in autoimmunity is the lack of surrogate biomarkers of immunological self-tolerance for disease monitoring. Here, we show that peripheral frequency of a regulatory T cell population, characterized by the co-expression of CD3 and CD56 molecules (TR3-56), is reduced in subjects with new-onset type 1 diabetes (T1D). In three independent T1D cohorts, we find that low frequency of circulating TR3-56 cells is associated with reduced β-cell function and with the presence of diabetic ketoacidosis. As autoreactive CD8+ T cells mediate disruption of insulin-producing β-cells1-3, we demonstrate that TR3-56 cells can suppress CD8+ T cell functions in vitro by reducing levels of intracellular reactive oxygen species. The suppressive function, phenotype and transcriptional signature of TR3-56 cells are also altered in T1D children. Together, our findings indicate that TR3-56 cells constitute a regulatory cell population that controls CD8+ effector functions, whose peripheral frequency may represent a traceable biomarker for monitoring immunological self-tolerance in T1D.
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