Moshe Arditi, M.D.
Executive Vice-Chair, Department of Pediatrics for Research
Professor of Pediatrics, Cedars Sinai Medical Center and UCLA School of Medicine
Director, Division of Pediatric Infectious Diseases and Immunology,
Director, Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Science, Cedars Sinai Medical Center, Los Angeles, CA, USA
Moshe Arditi, MD, is the executive vice-chair of the Department of Pediatrics for Research and the director of the Pediatric Infectious Diseases and Immunology Division at Cedars-Sinai. He is also director of the Infectious and Immunological Diseases Research Center in the Department of the Biomedical Sciences and a member of the Cedars-Sinai Smidt Heart Institute. The Arditi Laboratory has received National Institutes of Health (NIH) funding continuously for the past 24 years. The broad focus of the group is on innate immunity and host-pathogen interactions as they relate to acute and chronic inflammatory diseases. A major research focus of Arditi and his team is the discovery of the immunopathologic mechanisms that drive the development of cardiovascular lesions in Kawasaki disease vasculitis. The group uses a well-established and accepted experimental mouse model of Kawasaki disease vasculitis that recapitulates the coronary arteritis, abdominal aorta dilation, aneurysms, and myocarditis observed in human patients. Arditi was the first to discover that the intracellular signaling molecules in LPS-TLR4 signaling in endothelial cells are the same molecules that are used by IL-1b, including MyD88 (JBC, 1999). He discovered the role of TLR4 in atherosclerosis (PNAS, 2004), and made the seminal discovery that mitochondrial oxidative DNA damage plays a key role in the induction of NLRP3 inflammasome and secretion of IL-1beta (Immunity, 2012). Arditi’s seminal findings using this experimental mouse model demonstrated the key role of IL-1 beta in the cardiac manifestations of Kawasaki disease and led to ongoing phase II clinical trials using anti-IL-1 therapies in children with Kawasaki disease who are unresponsive to IVIG therapy. The Arditi lab also investigates the innate and adaptive immune mechanisms that contribute to atherosclerosis, including infection-mediated acceleration of atherosclerosis, the role of mitochondrial oxidative DNA damage, activation of the NLRP3 inflammasome, and the IL-1beta pathway. A recent discovery made by his laboratory includes the role of mitochondrial oxidative DNA binding and activating NLRP3 inflammasome for IL-1beta release. He is also pursuing the mechanisms for gender differences in inflammatory diseases, such as Kawasaki Disease vasculitis and atherosclerosis, as well as responses to therapy that may be gender-dependent. He and his collaborators at the University of Pittsburgh discovered the SARS-CoV2 Superantigen-like motif at the furin cleavage site of the spike protein that may bind TCR and MHCII to induce cytokine storm and may play a role in post-acute COVID-19 hyperinflammatory syndromes, such as MIS-C and MIS-A. Dr. Arditi has authored and co-authored more than 166 original articles in peer-reviewed publications. He is the recipient of the 2019 Pioneer of Medicine Award at Cedars-Sinai Medical Center.