Gabriel Nunez, MD

Professor, Department of Pathology
Paul de Kruif Professor

Subspecialty: Immunology/Inflammation
Email Address:
Office Phone: 764-8514
Fax: 734-647-9654
View Address


Brief Biography:

Gabriel Nuñez earned his M.D. degree from the University of Seville, Spain, in 1977. He received postdoctoral training in Immunology at the University of Texas Southwestern Medical Center, Dallas (1979–1984) and residency training in Anatomical Pathology at Washington University in St Louis (1985–1990). In 1987, he joined the laboratory of Stanley Korsmeyer at Washington University, where he studied the function of the anti-apoptotic protein BCL-2. In 1991, he joined the Department of Pathology at the University of Michigan in Ann Arbor as an Assistant Professor and was promoted to full Professor in 2001. He holds the Paul de Kruif Endowed Professorship in Academic Pathology. His laboratory identified NOD1 and NOD2, the first members of the Nod-like receptor (NLR) family, a class of pattern-recognition receptors that mediate cytosolic sensing of microbial organisms. Nuñez and colleagues showed that genetic variation in a NLR family member, NOD2, is strongly associated with susceptibility to Crohn's disease. Currently, the Nuñez laboratory is interested in signaling pathways regulating innate immunity, the pathogenesis of inflammatory disease and the role of the microbiota in host defense and colitis. Dr. Nuñez is the author of more than 270 scientific publications. His research program is supported by grants from the National Institutes of Health, the Broad Foundation, and the Crohn’s and Colitis Foundation of America.


Research Interests:

The Nuñez laboratory is interested in signaling pathways regulating innate immunity, the pathogenesis of inflammatory disease and cancer. Specifically, the research focuses on mechanistic studies to understand the role of pattern recognition receptors (PRRs) including Nod-like receptors (NLRs) and Toll-like receptors (TLRs) in the host immune response against microbial pathogens and endogenous damage signals. Current studies focus on models of intestinal, skin and lung inflammation driven by microbial pathogens, commensal bacteria and sterile organ injury. Several approaches that include analyses of genetically modified mutant mice and biochemical studies are used to determine mechanisms involved in the interaction between microbial/endogenous molecules and NLRs. Several NLR proteins including Nod2 and Nlrp3 are mutated in patients with inflammatory diseases (Crohn's disease and autoinflammatory syndromes). Studies to understand how NLR mutant proteins lead to disease are a major effort of the laboratory. In addition, the role of the microbiota in the colonization of enteric pathogens and pathogen-driven intestinal inflammation is being studied using germ-free animals.


Most Recent Publications: