Publications by authors named "E Karakoc-Aydiner"

Introduction: Listeria monocytogenes is a Gram-positive bacillus that causes severe infections mainly in newborns, pregnant women, immunocompromised individuals, and elderly. In this report, we present a case of immune dysregulation that presented with invasive Listeria infection despite the absence of these risk factors.

Case: A previously healthy 5-year-old girl developed L.

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Objective: Prolidase deficiency is a metabolic and immunological disorder that is inherited in an autosomal recessive manner. In prolidase deficiency, a broad spectrum of differences is observed in patients, ranging from asymptomatic to multisystem involvement. There is scarce information in the literature on the atypical features and immunophenotypes of this disease.

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Human recombination-activating gene (RAG) deficiency can manifest with distinct clinical and immunological phenotypes. By applying a multiomics approach to a large group of -mutated patients, we aimed at characterizing the immunopathology associated with each phenotype. Although defective T and B cell development is common to all phenotypes, patients with hypomorphic variants can generate T and B cells with signatures of immune dysregulation and produce autoantibodies to a broad range of self-antigens, including type I interferons.

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Children with milk and egg allergies have outcomes in which, three-quarters are tolerant to baked forms of the allergenic food. Identifying predictors of tolerance to baked foods for IgE-mediated immediate-type reactions may guide the early introduction of baked allergens to diet and tolerance development. This study explores factors associated with early tolerance to baked foods.

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Article Synopsis
  • STAT3 gain-of-function disease causes issues like immune system overactivity and growth problems, but long-term treatment with the JAK inhibitor ruxolitinib has shown promise in symptom relief.
  • The study monitored clinical and immune responses of four patients over a year, noting significant changes in T cell populations and the normalization of blood cell profiles, which were previously dysregulated.
  • Ruxolitinib treatment not only managed symptoms but also modified harmful immune cell characteristics and reduced certain auto-reactive T-cell clones, suggesting a potential pathway to better control the disease's impact.
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