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Sökning: WFRF:(Franckaert Dean)

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1.
  • Dooley, James, et al. (författare)
  • Genetic predisposition for beta cell fragility underlies type 1 and type 2 diabetes
  • 2016
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 48, s. 519-527
  • Tidskriftsartikel (refereegranskat)abstract
    • Type 1 (T1D) and type 2 (T2D) diabetes share pathophysiological characteristics, yet mechanistic links have remained elusive. T1D results from autoimmune destruction of pancreatic beta cells, whereas beta cell failure in T2D is delayed and progressive. Here we find a new genetic component of diabetes susceptibility in T1D non-obese diabetic (NOD) mice, identifying immune-independent beta cell fragility. Genetic variation in Xrcc4 and Glis3 alters the response of NOD beta cells to unfolded protein stress, enhancing the apoptotic and senescent fates. The same transcriptional relationships were observed in human islets, demonstrating the role of beta cell fragility in genetic predisposition to diabetes.
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2.
  • Franckaert, Dean, et al. (författare)
  • Premature thymic involution is independent of structural plasticity of the thymic stroma.
  • 2015
  • Ingår i: European journal of immunology. - : Wiley. - 1521-4141 .- 0014-2980. ; 45:5, s. 1535-1547
  • Tidskriftsartikel (refereegranskat)abstract
    • The thymus is the organ devoted to T-cell production. The thymus undergoes multiple rounds of atrophy and redevelopment before degenerating with age in a process known as involution. This process is poorly understood, despite the influence the phenomenon has on peripheral T-cell numbers. Here we have investigated the FVB/N mouse strain, which displays premature thymic involution. We find multiple architectural and cellular features that precede thymic involution, including disruption of the epithelial-endothelial relationship and a progressive loss of pro-T cells. The architectural features, reminiscent of the human thymus, are intrinsic to the non-hematopoietic compartment and are neither necessary nor sufficient for thymic involution. By contrast, the loss of pro-T cells is intrinsic to the hematopoietic compartment, and is sufficient to drive premature involution. These results identify pro-T-cell loss as the main driver of premature thymic involution, and highlight the plasticity of the thymic stroma, capable of maintaining function across diverse inter-strain architectures. This article is protected by copyright. All rights reserved.
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