A photo of Joseph Qualls.

Associate Professor, UC Department of Pediatrics


Biography & Affiliation


Dr. Qualls completed his undergraduate work in 2002, receiving his BA summa cum laude in biology from Thomas More College in Crestview Hills, KY. 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, TN, 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.

The Qualls laboratory is currently addressing the provocative role of L-arginine biosynthesis from L-citrulline during intracellular infection, how this mechanism is regulated at the cellular level (predominantly in macrophages and T cells), and the mechanism(s) of L-arginine/L-citrulline-mediated immune cell function. While greatly unexplored, this pathway of amino acid recycling and utilization is vital as mice deficient in L-arginine biosynthesis, compared to normal mice, lack efficient control of M. tuberculosis infection.

Academic Affiliation

Associate Professor, UC Department of Pediatrics


Infectious Diseases


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.


Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis. Boucher, AA; Rosenfeldt, L; Mureb, D; Shafer, J; Sharma, BK; Lane, A; Crowther, RR; McKell, MC; Whitt, J; Alenghat, T; et al. Journal of Thrombosis and Haemostasis. 2020; 18:91-103.

Macrophage Function in the Pathogenesis of Non-alcoholic Fatty Liver Disease: The Mac Attack. Oates, JR; McKell, MC; Moreno-Fernandez, ME; Damen, MS M A; Deepe, GS; Qualls, JE; Divanovic, S. Frontiers in Immunology. 2019; 10.

L-Arginine Synthesis from L-Citrulline in Myeloid Cells Drives Host Defense against Mycobacteria In Vivo. Lange, SM; McKell, MC; Schmidt, SM; Zhao, J; Crowther, RR; Green, LC; Bricker, RL; Arnett, E; Kohler, SE; Schlesinger, LS; et al. Journal of immunology (Baltimore, Md. : 1950). 2019; 202:1747-1754.

L-citrulline Metabolism in Mice augments cD4(+) T cell Proliferation and cytokine Production In Vitro, and accumulation in the Mycobacteria-infected lung. Lange, SM; McKell, MC; Schmidt, SM; Hossfeld, AP; Chaturvedi, V; Kinder, JM; McAlees, JW; Lewkowich, IP; Way, SS; Turner, J; et al. Frontiers in Immunology. 2017; 8.

CD44 variant isoform 9 emerges in response to injury and contributes to the regeneration of the gastric epithelium. Bertaux-Skeirik, N; Wunderlich, M; Teal, E; Chakrabarti, J; Biesiada, J; Mahe, M; Sundaram, N; Gabre, J; Hawkins, J; Jian, G; et al. The Journal of pathology and bacteriology. 2017; 242:463-475.

T Cells Encountering Myeloid Cells Programmed for Amino Acid-dependent Immunosuppression Use Rictor/mTORC2 Protein for Proliferative Checkpoint Decisions. Van de Velde, L; Subramanian, C; Smith, AM; Barron, L; Qualls, JE; Neale, G; Alfonso-Pecchio, A; Jackowski, S; Rock, CO; Wynn, TA; et al. The Journal of biological chemistry. 2017; 292:15-30.

T Cell Cancer Therapy Requires CD40-CD40L Activation of Tumor Necrosis Factor and Inducible Nitric-Oxide-Synthase-Producing Dendritic Cells. Marigo, I; Zilio, S; Desantis, G; Mlecnik, B; Agnellini, AH R; Ugel, S; Sasso, MS; Qualls, JE; Kratochvill, F; Zanovello, P; et al. Cancer Cell. 2016; 30:377-390.

Immunometabolism within the tuberculosis granuloma: amino acids, hypoxia, and cellular respiration. Qualls, JE; Murray, PJ. Springer Seminars in Immunopathology. 2016; 38:139-152.

Differential Requirements for L-Citrulline and L-Arginine during Antimycobacterial Macrophage Activity. Rapovy, SM; Zhao, J; Bricker, RL; Schmidt, SM; Setchell, KD R; Qualls, JE. Journal of immunology (Baltimore, Md. : 1950). 2015; 195:3293-3300.

TNF Counterbalances the Emergence of M2 Tumor Macrophages. Kratochvill, F; Neale, G; Haverkamp, JM; Van de Velde, L; Smith, AM; Kawauchi, D; McEvoy, J; Roussel, MF; Dyer, MA; Qualls, JE; et al. Cell Reports. 2015; 12:1902-1914.