Joseph E. Qualls, PhD

Assistant Professor, UC Department of Pediatrics

Phone: 513-636-9102


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Immunology; innate immunity; macrophage biology; amino acid metabolism; intracellular pathogenesis 


Dr. Qualls completed his undergraduate work in 2002, receiving his BA summa cum laude in biology from Thomas More College in Crestview Hills, Kentucky. He then joined the laboratory of Don Cohen, PhD, in the Department of Microbiology, Immunology and Molecular Genetics at the University of Kentucky, where he studied the role of macrophages and dendritic cells during the development of inflammatory bowel disease. After defending his thesis and receiving his PhD in 2007, Dr. Qualls began his postdoctoral training with Peter Murray, PhD, in the Department of Infectious Diseases and Immunology at St. Jude Children’s Research Hospital in Memphis, Tennessee, where his research helped to define the functional plasticity of macrophages in response to infection and cancer. During his postdoctoral training, Dr. Qualls received a Ruth L. Kirschstein National Research Service Award and actively participated as vice chair of Mentoring Activities within the Postdoctoral Association Council and as a member of the Education Programs Committee.

Dr. Qualls’ long-term goals are to understand the interplay between nutrition, metabolism and immune regulation during anti-pathogen defense. He has focused on how macrophages use the amino acid, L-arginine, to combat intracellular pathogens. As a starting point to appreciate broader principles of immunity and metabolism he established a map of L-arginine metabolism at the transcriptomic and metabolomic levels. His laboratory now uses this map to dissect how L-arginine generates anti-microbial effectors, how this pathway is regulated, and how microbes can hijack the pathway. His current research has two complementary tracks that retain initial focus on L-arginine metabolism in macrophages, but will eventually broaden into larger issues concerning metabolism in immunity.

Current research: Many groups have shown that T cell function is inhibited via byproducts of L-arginine metabolism or when extracellular L-arginine becomes limiting. In one project, the laboratory is focused on characterizing the in vivo function of L-arginine utilization by macrophages during mycobacterial infection, and how this affects anti-pathogen T cell function. In parallel, the laboratory is addressing the provocative role of L-arginine biosynthesis from L-citrulline during intracellular infection, and how this mechanism is regulated at the cellular level. While greatly unexplored, this pathway of amino acid recycling is vital as mice deficient in L-arginine biosynthesis, compared to normal mice, lack efficient control of both M. bovis BCG and M. tuberculosis infection.

Education and Training

BA: Thomas More College, Crestview Hills, KY, 2002.

PhD: University of Kentucky, Lexington, KY, 2007.

Postdoctoral Fellowship: St. Jude Children’s Research Hospital, Memphis, TN, 2012.


View PubMed Publications


Consequences of amino acid limitation on immune function. Principle Investigator. Cincinnati Children’s TAPS Program, Trustee Award. Jan. 2013 – Dec. 2014.