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GDCB Seminar — "Developmental programming of health and disease: the effects of extrinsic inputs on developmental hematopoiesis"

Oct 1, 2024 - 1:00 PM
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Anna Beaudin, University of Utah associate professor

 

 

 

 

 

 

Speaker — Anna Beaudin, University of Utah School of Medicine 

  • associate professor and associate chief of basic research in the Division of Hematology and Hematologic Malignancies
  • director in NIDDK-Utah Center for Iron and Heme Disorders
  • adjunct associate professor, Departments of Pathology and Human Genetics

Title — "Developmental programming of health and disease: the effects of extrinsic inputs on developmental hematopoiesis"

Abstract — The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that risk for poor health outcomes and chronic disease can be traced to perturbations during early life. It is now well recognized that immune dysfunction is an important driver of pathology in many chronic diseases. Our lab’s work broadly aims to link early life perturbation of the developing hematopoietic system with immune dysfunction as a driver of pathogenesis in various contexts. We approach this by investigating how developmental perturbation, including prenatal inflammation, early-life infection, and modulation of prenatal nutrition affects disease susceptibility from two angles: first, we investigate how developmental perturbation influences the fate and function of developing hematopoietic stem cells into the postnatal period. Second, we investigate how the same perturbations influence the production of specialized immune cells produced only during fetal life that persist and contribute to adult immunity. These specialized fetal-derived immune cells seed and take up residence in developing tissues, where they regulate tissue development and tissue homeostasis, in addition to tissue immunity. Our studies highlight how heterogeneity of the fetal hematopoietic stem and progenitor compartment underlies diverse responses to inflammatory stimuli during development and influence postnatal immunity. Furthermore, our data reveal how sustained programming of fetal-derived immune cells in response to inflammation can remodel tissue immunity and function and drive susceptibility to disease.  

Hosts — Clyde Campbell and Raquel Espin Palazon, genetics, development and cell biology assistant professors