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Kasper Hoebe, PhDAssistant Professor Department of Pediatrics; Division of Cellular and Molecular Immunology
Dr. Hoebe’s research is focused on a better understanding of the genes required for a normal immune system. Specifically, his work focuses on the interaction between NK cells and their role in the onset of adaptive immune responses including CD8+ T CD4+ T and B cell responses. NK cells are able to recognize a variety of target cells, including tumor cells, stressed cells or infected cells, via receptor –mediated interactions involving "missing self", "induced self" or recognition of pathogen-derived molecules. Upon administration of antigen-expressing cells that exhibit "missing self", NK cells induce cell death and subsequently prompt a strong CD8+ T, CD4+ T and B cell response. Dr. Hoebe’s laboratory applies a forward genetic approach using ENU mutagenesis to identify key components in NK cell function and subsequent CD8+ T cell responses via the above described cell death pathway. Using this approach, his laboratory has identified a number of germline mutants that are NK and/or CD8+ T cell-deficient. As part of this approach he identified a mutant—designated sphinx—that exhibited a complete lack of peripheral NK and CD8+ T cells. In addition, these mice developed liver disease and colitis and had an overall poor survival. His laboratory aims to identify the genetic basis for such severe immunological phenotypes and ultimately gain important insight into gene function and their relation to disease development.
Dr. Hoebe collaborates with the following Digestive Health Center members Drs. Bezerra, Denson, Karp, and Steinbrecher. Anticipated use of Cores: Integrative Morphology and Gene and Protein Expression Cores.
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Antibiotic treatment abrogates colitis but not lymphopenia and liver extramedullary hematopoiesis in Gimap5sph/sph mice. H&E-stained sections from the colons and livers of 9-wk-old co-housed mice assessed for extramedullary hematopoiesis and intestinal inflammation. Figure from J Immunol, 2010;184:3743-3754.
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