Joseph E. Qualls, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-9102

Email joseph.qualls@cchmc.org

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

Visit the Qualls Lab.

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.

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

Lange SM, McKell MC, Schmidt SM, Zhao J, Crowther RR, Green LC, Bricker RL, Arnett E, Köhler SE, Schlesinger LS, Setchell KDR, Qualls JE. L-Arginine Synthesis from L-Citrulline in Myeloid Cells Drives Host Defense against Mycobacteria In Vivo. J Immunol. 2019 Mar 15;202(6):1747-1754. Featured article. 

Lange SM, McKell MC, Schmidt SM, Hossfeld AP, Chaturvedi V, Kinder JM, McAlees JW, Lewkowich IP, Way SS, Turner J, Qualls JE. L-Citrulline Metabolism in Mice Augments CD4(+) T Cell Proliferation and Cytokine Production In Vitro, and Accumulation in the Mycobacteria-Infected Lung. Front Immunol. 2017 Nov 16;8:1561.  

Marigo I, Zilio S, Desantis G, Mlecnik B, Agnellini AH, Ugel S, Sasso MS, Qualls JE, Kratochvill F, Zanovello P, Molon B, Ries CH, Runza V, Hoves S, Bilocq AM, Bindea G, Mazza EM, Bicciato S, Galon J, Murray PJ, Bronte V. T Cell Cancer Therapy Requires CD40-CD40L Activation of Tumor Necrosis Factor and Inducible Nitric-Oxide-Synthase-Producing Dendritic Cells. Cancer Cell. 2016 Sep 12;30(3):377-90.

Rapovy SM, Zhao J, Bricker RL, Schmidt SM, Setchell KDR, Qualls JE. Differential requirements for L-citrulline and L-arginine during anti-mycobacterial macrophage activity. Journal of Immunology. 2015 Oct 1;195(7):3293-300.

Kratochvill F, Neale G, Haverkamp JM, Van de Velde L, Smith AM, Kawauchi D, McEvoy J, Roussel MF, Dyer MA, Qualls JE, Murray PJ. TNF counterbalances the emergence of M2 tumor macrophages. Cell Reports. 2015 Sep 22;12(11):1902-14.

Haverkamp JM, Smith AM, Weinlich R, Dillon CP, Qualls JE, Neale G, Koss B, Kim Y, Bronte V, Herold MJ, Green DR, Opferman JT, Murray PJ. Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways. Immunity. 2014 Dec 18;41(6):947-59.

Duque-Correa MA, Kuhl A, Rodriquez PC, Zedler U, Schommer-Leitner S, Rao M, Weiner J, Hurwitz R, Qualls JE, Kosmiadi GA, Murray PJ, Kaufmann SHE, Reece ST. Macrophage arginase-1 controls bacterial growth and pathology in hypoxic tuberculosis granulomas. Proceedings of the National Academy of Sciences – USA. 2014 Sep 23;111(38):E4024-32.

Qualls JE, Subramanian C, Smith AM, Balouzian L, DeFreitas AA, Shirey KA, Reutterer B, Kernbauer E, Stockinger S, Decker T, Miyairi I, Vogel SN, Rock CO, Murray PJ. Sustained generation of nitric oxide and control of mycobacterial infection requires argininosuccinate synthase 1. Cell Host & Microbe. 2012 Sep 13;12(3):313-23.

Qualls JE, Neale G, Smith AM, Koo MS, DeFreitas AA, Zhang H, Kaplan G, Watowich SS, Murray PJ. Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling. Science Signaling. 2010 Aug 17;3(135):ra62.

El Kasmi KC, Qualls JE (co-primary author), Pesce JT, Smith AM, Thompson RW, Henao-Tamayo M, Basaraba RJ, König T, Schleicher U, Koo M, Kaplan G, Fitzgerald KA, Tuomanen EI, Orne IM, Kanneganti T, Bogdan C, Wynn TA, Murray PJ. TLR-induced Arginase 1 thwarts effective immunity against intracellular pathogens. Nature Immunology. 2008 Dec;9(12):1399-406.

L-citrulline and anti-tuberculosis host defense. Principal Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases. July 2016-June 2021.