Publications by authors named "I Bulder"

Type 3 innate lymphoid cells (ILC3) are important in tissue homeostasis. In the gut, ILC3 repair damaged epithelium and suppress inflammation. In allogeneic hematopoietic cell transplantation (HCT), ILC3 protect against graft-versus-host disease (GvHD), most likely by restoring tissue damage and preventing inflammation.

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Introduction: Neutrophils promote chronic inflammation and release neutrophil extracellular traps (NETs) that can drive inflammatory responses. Inflammation influences progression of sickle cell disease (SCD), and a role for NETs has been suggested in the onset of vaso-occlusive crisis (VOC). We aimed to identify factors in the circulation of these patients that provoke NET release, with a focus on triggers associated with hemolysis.

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Article Synopsis
  • - The study investigates the role of cell-free DNA (cfDNA) and nucleosomes in acute Graft-versus-Host Disease (aGvHD) following allogeneic hematopoietic stem cell transplantation (HSCT), which can be a serious complication.
  • - Researchers found that in patients with aGvHD, nucleosome levels in plasma significantly increased at the time of diagnosis, alongside other known aGvHD markers, and similar results were observed in a mouse model.
  • - The findings indicate that cfDNA primarily comes from human donor cells and confirms its potential as an additional marker for aGvHD diagnosis and monitoring.
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Background: Platelet transfusions can be associated with adverse reactions, such as febrile non-haemolytic transfusion reaction (FNHTR). It has been suggested that damage-associated molecular patterns (DAMP) and complement play a role in FNHTR. This study investigated the nature of DAMPs and complement activation products contained in platelet concentrates during storage, with a specific focus on different platelet storage solutions.

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Article Synopsis
  • Circulating histones are linked to inflammatory diseases due to their cytotoxic effects, but it's unclear if histones and nucleosomes have the same level of toxicity.
  • The study found that factor VII-activating protease (FSAP) can neutralize histone cytotoxicity in cultured cells by degrading free histones, particularly when activated by contact with histones in serum.
  • Results showed that nucleosome-bound histones were less cytotoxic compared to free histones, and in patients with sepsis, histone H3 was mostly found in nucleosomes, indicating limited circulation of free histone H3.
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