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Faculty Profile Last Modified Time: 09:09:24 AM Wed, 25 Mar 2020   Contact Information Katherine King Associated Profiles  Professor, Pediatrics-Infectious Disease, Baylor College of Medicine   Mail Box: BCM320, Feigin Center, Room No.: TXFC-1150    kyk@bcm.edu     (832) 824-4330    Web Link    Lab Webpage    Stem Cells, Stem Cell Differentiation, Flow Cytometry, Hematopoeitic Stem Cells, Hematopoeisis, Interferon-Alpha, Gastrointestinal Microbiome, Anemia    Associated Profiles Professional Preparation Research and Expertise Affiliations Appointments  Professional Preparation  Degree Major Institution Year  MD, PhD Molecular Microbiology and Microbial Pathogenesis Washington University 2003  AB Biochemical Sciences Harvard University 1996  Research and Expertise Research Interests   Bone marrow suppression and pancytopenia can result from chronic inflammation. Bone marrow suppression is a risk factor for increased mortality for patients with chronic infections14-17 and aplastic anemia18-21. However, very little is known about the mechanisms by which inflammatory cytokines affect the hematopoietic progenitors that reside in bone marrow. We discovered that interferon gamma (IFN³) promotes hematopoietic stem cell (HSC) division and myeloid differentiation in a mouse model of Mycobacterium avium infection1. While this response can be helpful in the short term, it may be deleterious over the long term, with prolonged inflammation leading to stem cell exhaustion2. We have previously demonstrated that interferons, a class of inflammatory cytokines, directly activate hematopoietic stem cells (HSCs) to divide (Nature 2010). HSCs are the precursors of all cells of the peripheral blood, and they usually reside in a quiescent state in the bone marrow. Our work is among the first to demonstrate that inflammatory signaling can directly activate HSCs. Impaired quiescence mechanisms during long-term interferon stimulation result in differentiation and exhaustion of the HSC pool (Blood 2011, Stem Cells 2014). We recently demonstrated that chronic infection depletes HSCs through excessive terminal differentiation, in part mediated by the transcription factor Batf2 (Cell Reports 2016). Meanwhile, basal inflammatory signaling mediated through the intestinal microbiome is required to maintain normal blood homeostasis (Blood, 2017). Ongoing work is focused on defining molecular pathways underlying these phenomena. This knowledge is a key to understanding the pathophysiology of bone marrow failure syndromes and will likely provide novel targets for drug development. Furthermore, this work may elucidate how inflammatory signals affect the pattern of HSC differentiation as well as how infections can contribute to aging and oncogenesis.  Publications/Creative Works Click here to search for this faculty member's publications on PubMed.  Affiliations  Research Consortia Gulf Coast Cluster for Single Cell Omics Gulf Coast Cluster for Immunology  Appointments Title Department / School Institution Associate Professor Pediatrics-Infectious Disease Baylor College of Medicine Co-Director medical Scientist Training Program Baylor College of Medicine Steering Committee Pediatrician Scientist Training and Development Program Baylor College of Medicine

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