Our Labs

Mary Dinauer, MD, PhD, studies the superoxide-generating leukocyte NADPH oxidase and the role of oxidant production by neutrophils and macrophages in microbial killing, the inflammatory response, and autoimmunity. Inactivating mutations in the NADPH oxidase result in chronic granulomatous disease (CGD), a primary immunodeficiency associated with recurrent bacterial and fungal infections as well as a variety of chronic inflammatory disorders, including inflammatory bowel disease and discoid lupus. Moreover, hypomorphic NADPH oxidase gene variants are now linked to inflammatory bowel disease and autoimmunity. These clinical manifestations reflect the dual importance of the NADPH oxidase both for microbial killing and for negatively regulating cellular processes that limit inflammation by redox mechanisms.

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Our research focuses on the interface between the host innate immune system and large double-stranded DNA viruses and how interactions at this interface may influence the initiation of inappropriate autoimmune responses in rheumatic diseases. We are particularly interested in natural killer (NK) cells, innate lymphocytes that play a critical role in early anti-pathogen host defense…

Research profile

Research in our lab is focused on traumatic brain injury (TBI). Specifically, we are focused on utilizing clinical relevant animal models of TBI to study the effects of secondary insults — intracranial hypertension, hypoxemia and neuroinflammation — after moderate and severe TBI.

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Our research team studies the epidemiology, microbial virulence mechanisms and host defenses against community-associated methicillin-resistant staphylococcus aureus (CA-MRSA) colonization and disease.

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Research profile

Gooch’s main research interests are clinically studying skeletal dysplasias and orofacial clefting. She has a particular interest in disorders of FGFR3, such as achondroplasia and hypochondroplasia, as well as collagenopathies.

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Cancer develops through accumulation of DNA mutations and structural aberrations collectively known as genome instability. Genome damage in adult-onset malignancies can be traced to exogenous carcinogens or simply the process of aging. However, pediatric cancers do not arise as a result of aging or exogenous genotoxic agents. We are interested in the etiology of genome instability in pediatric cancers and the resulting genome-protective responses — also called DNA damage responses — that are activated. Our long-term goal is to identify predictors of mutagenesis and therapeutic vulnerabilities within DNA damage response pathways in order to develop new treatment options for children with cancer.

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The Greer lab is interested in how non-genetic information, termed epigenetics, regulates complex physiological and pathological phenotypes across generations.

Our lab’s overall focus is to understand how vascular elastic fibers, large arteries’ main extracellular matrix, develop and how abnormalities in their development lead to diseases such as aneurysms and hypertension.

Research profile

Work in our lab focuses on the integrated use of epidemiology, bioinformatics, and molecular virology to address questions in the developing childhood gut.

Research profile