Michael Dee Gunn, MD

Professor of Medicine
Professor in Immunology
Associate Professor in Pathology
Member of the Duke Cancer Institute
Campus mail CARL Building Room 180B, Durham, NC 27703
Phone (919) 681-0840
Email address michael.gunn@duke.edu

The focus of my work is on understanding how dendritic cells, monocytes, and macrophages regulate immune responses, contribute to specific disease pathologies, and can be manipulated to stimulate or inhibit specific immune responses. We are also using our knowledge of immunology to develop diagnostics and therapeutics for a variety of human diseases. 

Lab History 

The lab started with our discovery of the lymphoid chemokines, which regulate the migration of lymphocytes and dendritic cells to and within secondary lymphoid organs.  We identified the chemokine (CCL21) that mediates the entry of naïve T cells and activated dendritic cells into lymph nodes and the chemokine (CXCL13) that mediates the entry of B cells into lymphoid follicles.  Our focus then shifted to understanding how specific cell types, primarily dendritic cells, and cell migration events regulate immune responses.  We identified murine plasmacytoid dendritic cells, the cell type that causes pulmonary immune pathology during influenza infection, the dendritic cell type that stimulates Th1 immune responses, and the cell type that induces neuronal injury in Alzheimer's disease.  Our current work continues these basic studies while applying our findings to models of human disease. 

Current Research 

Identification and characterization of inflammatory cell populations in models of human disease – We have developed advanced methods of flow cytometric analysis that allows us to quantify and fully characterize all inflammatory cell types in murine and human tissues.  Using these methods, we are working to identify the cells that mediate a variety of immune pathologies.  Examples include the identification of immune-stimulatory and immune-suppressive cell types in brain tumors, identification of the cells that induce vascular changes pulmonary hypertension, and characterization of the inflammatory response to a variety of infectious pathogens.

Tumor immune therapeutics – We have developed a novel cellular vaccine strategy for the treatment of cancer.  This strategy is much simpler, more cost effective, more clinically feasible, and much more efficacious than classic dendritic cell vaccines.  We are now testing this vaccine in various preclinical tumor models including melanoma and glioblastoma and will soon be advancing it to initial human clinical trials.

Treatment of Acute Lung Injury – We have identified the first small molecule pharmacologic agent that is effective in reducing respiratory dysfunction, vascular leak, tissue injury, and mortality during Acute Lung Injury.  We are currently validating this agent in animal models of chemical-induced ALI and testing its efficacy in reducing ALI caused by other agents such as influenza and smoke inhalation.  We hope to develop this agent as the first effective pharmacologic treatment for ALI in humans.

Development of recombinant antibodies as diagnostic reagents – Our lab has developed novel methods to generate recombinant single chain antibodies using phage display technology.  We are currently using these methods to generate pathogen-specific antibodies for use in diagnostic tests for a variety of human bacterial, viral, and fungal infections.  In collaboration with Duke Biomedical Engineering, we are testing the use of our antibodies in a novel diagnostic assay platform to develop point-of-care assays for the diagnosis of infections by agents such as Zika virus, Dengue virus, Salmonella typhi, and Aspergillus fumigatus.

Education and Training

  • Fellowship in Cardiology, Cardiology, University of California, San Francisco, 0018
  • Internship and Residency, Internal Medicine, Parkland Health & Hospital System, 0018
  • M.D., UT Southwestern Medical School, 1983


Hart, Justin P., Michael D. Gunn, and Salvatore V. Pizzo. “A CD91-positive subset of CD11c+ blood dendritic cells: characterization of the APC that functions to enhance adaptive immune responses against CD91-targeted antigens.” J Immunol 172, no. 1 (January 1, 2004): 70–78. https://doi.org/10.4049/jimmunol.172.1.70.

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McLachlan, James B., Justin P. Hart, Salvatore V. Pizzo, Christopher P. Shelburne, Herman F. Staats, Michael D. Gunn, and Soman N. Abraham. “Mast cell-derived tumor necrosis factor induces hypertrophy of draining lymph nodes during infection.” Nat Immunol 4, no. 12 (December 2003): 1199–1205. https://doi.org/10.1038/ni1005.

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Honig, Shaun M., Shuang Fu, Xia Mao, Adam Yopp, Michael D. Gunn, Gwendalyn J. Randolph, and Jonathan S. Bromberg. “FTY720 stimulates multidrug transporter- and cysteinyl leukotriene-dependent T cell chemotaxis to lymph nodes.” J Clin Invest 111, no. 5 (March 2003): 627–37. https://doi.org/10.1172/JCI16200.

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Wigle, Jeffrey T., Natasha Harvey, Michael Detmar, Irina Lagutina, Gerard Grosveld, Michael D. Gunn, David G. Jackson, and Guillermo Oliver. “An essential role for Prox1 in the induction of the lymphatic endothelial cell phenotype.” Embo J 21, no. 7 (April 2, 2002): 1505–13. https://doi.org/10.1093/emboj/21.7.1505.

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Gunn, M. D., M. Yanagita, and H. Nakano. “Identification and characterization of murine plasmacytoid dendritic cells.” Faseb Journal 16, no. 5 (March 22, 2002): A1230–31.


Red-Horse, K., P. M. Drake, M. D. Gunn, and S. J. Fisher. “Chemokine ligand and receptor expression in the pregnant uterus: reciprocal patterns in complementary cell subsets suggest functional roles.” Am J Pathol 159, no. 6 (December 2001): 2199–2213. https://doi.org/10.1016/S0002-9440(10)63071-4.

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Nakano, H., M. Yanagita, and M. D. Gunn. “CD11c(+)B220(+)Gr-1(+) cells in mouse lymph nodes and spleen display characteristics of plasmacytoid dendritic cells.” J Exp Med 194, no. 8 (October 15, 2001): 1171–78. https://doi.org/10.1084/jem.194.8.1171.

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Drake, P. M., M. D. Gunn, I. F. Charo, C. L. Tsou, Y. Zhou, L. Huang, and S. J. Fisher. “Human placental cytotrophoblasts attract monocytes and CD56(bright) natural killer cells via the actions of monocyte inflammatory protein 1alpha.” J Exp Med 193, no. 10 (May 21, 2001): 1199–1212. https://doi.org/10.1084/jem.193.10.1199.

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Mori, S., H. Nakano, K. Aritomi, C. R. Wang, M. D. Gunn, and T. Kakiuchi. “Mice lacking expression of the chemokines CCL21-ser and CCL19 (plt mice) demonstrate delayed but enhanced T cell immune responses.” J Exp Med 193, no. 2 (January 15, 2001): 207–18. https://doi.org/10.1084/jem.193.2.207.

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