Text Image: UM Medical School: Graduate Program in Immunology
Text Image: Faculty

Gabriel Nuñez, M.D.
Paul de Kruif Endowed Professor,
Department of Pathology
bclx@umich.edu

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 and skin 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.  Another line of investigation is the role of the microbiota in the colonization of enteric pathogens and pathogen-driven intestinal inflammation. 

 

Representative Publications

Kim YG, Kamada N., Shaw MH, Warner N., Chen GY, Franchi L., and Núñez G. Nod2 Orchestrates Immune Responses that Promote Intestinal Pathogen Eradication via CCL2-Dependent Recruitment of Inflammatory Monocytes. Immunity 34:769-780 (2011).

Kim YG, Park J-H, Reimer T, Baker DP, Kawai T, Kumar H, Shizuo Akira S,Wobus C, and Núñez G. Nod1 and Nod2 Signaling Augmented by Viral Infection through Type I Interferons Potentiate Lethality Induced by Secondary Bacterial Infection. Cell Host & Microbe 16;496-507 (2011).

Shaw MH, Kamada N, Kim YG, Núñez G. Microbiota-induced IL-1β, but not IL-6, is critical for the development of steady-state TH17 cells in the intestine. J Exp Med. 209:251-258 (2012). PMID: 22291094.

Franchi L, Kamada N, Nakamura Y, Burberry A, Kuffa P, Suzuki S, Shaw M. H., Kim Y-G., and Núñez G. NLRC4-driven IL-1β Production Discriminates Between Pathogenic and Commensal Bacteria and Promotes Host Defense in the Intestine. Nature Immunol. 13:449-456 (2012).

Kamada N. Kim YG, Sham HP, Vallance BA, Puente JL, Martens EC, Núñez G.  Regulated virulence controls the ability of a pathogen to compete with the gut microbiota. Science 336:1325, (2012).

Nakamura  Y, Luigi Franchi L, Kambe N, Meng G, Strober Wand, Gabriel Núñez G. Critical Rolefor Mast Cells in IL-1β-Driven Skin Inflammation Induced by an Activating Nlrp3 mutation. Immunity, 37, 1–11 (2012).

Franchi L, Kamada N, Nakamura Y, Burberry A, Kuffa P, Suzuki S, Shaw M. H., Kim Y-G., and Núñez G. NLRC4-driven IL-1 Production Discriminates Between Pathogenic and Commensal Bacteria and Promotes Host Defense in the Intestine. Nature Immunology 13:449-456 (2012). PMCID: PMC3395620.

Munoz-Planillo R, Kuffa P, Martinez-Colon G, Smith B.L., Rajendiran T.M.,
Núñez G. K+ Efflux Is the Common Trigger of NLRP3 Inflammasome Activation by Bacterial Toxins and Particulate Matter. Immunity 38:1142-1153 (2013). PMCID: PMC3730833.

Nakamura Y, Oscherwitz J, Cease KB, Chan SM, Muñoz-Planillo R, Hasegawa M, Villaruz AE, Cheung GY, McGavin MJ, Travers JB, Otto M, Inohara N,
Núñez G. Staphylococcus δ-toxin induces allergic skin disease by activating mast cells. Nature 503(7476):397-401 (2013). PMID: 24172897.

Burberry A, Zeng MY, Ding L, Wicks I, Inohara N, Morrison SJ,
Núñez G. Infection Mobilizes Hematopoietic Stem Cells through Cooperative NOD-like Receptor and Toll-like Receptor Signaling. Cell Host & Microbe, In Press. PMID: 24882704; PubMed Central PMCID: PMC4085166

 

 

 


About Us
| Research Opportunities | Faculty | Graduate Students | Admissions | Coursework | Immunology Seminars | Life in A2
UM Gateway | UM Medical School | Program in Biological Sciences | UM Health System
Web Design by BMC Media

Copyright © 2002 The Regents of the University of Michigan