We know so much about the human body, yet the science of medicine holds many mysteries. This couldn’t be truer for allergic and immune conditions, many of which have origins in childhood and cause immense suffering.
In my clinical practice and laboratory at Cincinnati Children’s Hospital Medical Center, I am focused on solving the mysteries of allergic inflammatory disease, especially eosinophilic gastrointestinal disorders, or EGIDs.
I had the opportunity early in my training to work alongside wonderful mentors who supported me and my interests in this work. At Brandeis University, I worked under the guidance of the late Professor William P. Jencks, a renowned biochemist, and learned the basic tenets of scientific inquiry. Under the direction of Harvard Medical School’s Dr. Frank Austen, I conducted studies on eosinophil hematopoiesis and developed the first culture system for human eosinophils. During my post-doctoral training with Harvard’s renowned geneticist Dr. Philip Leder, I cloned the eotaxin chemokine.
These were such exciting times for me as a young scientist, and these positive training experiences formed the foundation on which I have built my own laboratory at Cincinnati Children’s.
Here, our mission is to improve the health and well-being of children with allergic and immune conditions. We do this through innovative research, outstanding clinical care, and education of the current and next generation of leaders in healthcare and research.
We take a multidisciplinary approach to our work and have developed preclinical models that have taught us more about the genetics, genomics, molecular immunology and biochemistry of eosinophilic diseases. We have also built translational experimental systems that help us better understand human disease. These approaches have laid the foundation for our clinical trials in patients.
My approach to patients is to provide the best care possible while learning from each patient through research.
With the support of my team, I have been awarded a National Institutes of Health Merit Award, the Cincinnati Children's Hospital Research Achievement Award, and have been elected as a member of both the American Society for Clinical Investigation and the American Association for the Advancement of Science. I am President-Elect of the International Eosinophil Society and hope to use this experience to positively influence future research and care for eosinophilic disease.
I am pleased to see my research advance the understanding and treatment of allergic diseases. At the same time, I know that we need to do much more.
I dream of a day when we can re-educate the immune system to reverse the food hypersensitivity that drives EGIDs and that such treatments will be readily affordable and available.
I am fortunate at Cincinnati Children’s to be surrounded by a dedicated and like-minded team of scientists and clinicians – all determined to develop the best treatment for eosinophilic diseases. And I am forever grateful to all of the children, parents, families and adults who partner with us in our efforts to conquer eosinophilic diseases. I am also grateful to my wife and my parents for their love, support and encouragement.
We have accomplished so much, and I look forward to seeing how our contributions can contribute to positively impacting the emerging breakthroughs in diagnosing and treating patients.
MD, PhD: Harvard Medical School, Cambridge, MA, 1990.
Residency: Pediatrics, Children's Hospital, Boston, MA, 1991-1992.
Fellowship: Immunology / Allergy, Children's Hospital, Boston, MA, 1992-1994; Hematology / Oncology, Children's Hospital and Dana Farber Cancer Institute, Boston, MA, 1992-1995.
Certification: National Board of Medical Examiners, 1991; Board of Registration in Medicine, MA, 1992; American Board of Pediatrics, 1995, 2001, 2008; Ohio State Medical Board, 1997; American Board of Allergy and Immunology, 1997, 2006.
Allergy and Immunology, Eosinophilic Disorders
Allergy and Immunology, Eosinophilic Disorders, Global Health
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Single-cell RNA sequencing identifies inflammatory tissue T cells in eosinophilic esophagitis. The Journal of Clinical Investigation. 2019; 129:2014-2028.
Chromatin regulates IL-33 release and extracellular cytokine activity. Nature Communications. 2018; 9:3244.
Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study. The Lancet Gastroenterology and Hepatology. 2018; 3:477-488.
The antiprotease SPINK7 serves as an inhibitory checkpoint for esophageal epithelial inflammatory responses. Science Translational Medicine. 2018; 10.
Eosinophilic esophagitis (EoE) genetic susceptibility is mediated by synergistic interactions between EoE-specific and general atopic disease loci. Journal of Allergy and Clinical Immunology. 2018; 141:1690-1698.
Cadherin 26 is an alpha integrin-binding epithelial receptor regulated during allergic inflammation. Mucosal Immunology. 2017; 10:1190-1201.
Genome-wide association analysis of eosinophilic esophagitis provides insight into the tissue specificity of this allergic disease. Nature Genetics. 2014; 46:895-900.
Molecular diagnosis of eosinophilic esophagitis by gene expression profiling. Gastroenterology. 2013; 145:1289-1299.
The minichromosome maintenance complex drives esophageal basal zone hyperplasia. JCI insight. 2023; 8:e172143.
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