Donghai Wang, PhD

Assistant Professor in Medicine
Assistant Professor in Immunology
Member of the Duke Cancer Institute
Campus mail Rm 214a, Edwin Jones Building, 207 Research Drive, Durham, NC 27710
Phone (919) 684-5586
Email address donghai.wang@duke.edu

Inflammation underlies a variety of human diseases such as obesity, diabetes, cardiovascular diseases, neurodegenerative diseases, arthritis and cancer. Together, these diseases constitute a major challenge to the well being of modern human society. Understanding the fundamental mechanisms of inflammation may provide rationales for designing novel interventions to treat these maladies. Autoinflammatory diseases are an emerging family of illness, characterized by dysregulation of innate immune responses. Studies of these hereditary human disorders have provided invaluable insight into basic cellular and molecular mechanisms of the innate immune responses and have contributed significantly to the development of targeted therapies for common human inflammatory diseases such as arthritis. My long term goal is to understand the pathophysiological mechanisms of autoinflammatory diseases and to apply knowledge from such studies to develop novel treatment of inflammatory human diseases. Our recent studies of one of such diseases, namely mevalonate kinase deficiency, has allowed us to unravel the unexpected connection between the cholesterol-biosynthesis mevalonate pathway and toll like receptor (TLR)-mediated phosphatidyl inosital 3(PI3)-kinase signaling. These exciting new discoveries will greatly advance our knowledge of innate immune signaling and may provide clues for new interventions of a variety of human diseases.

Education and Training

  • Ph.D., Sun Yat Sen University (China), 2004

Publications

Yang, B, Suwanpradid, J, Sanchez-Lagunes, R, Choi, HW, Hoang, P, Wang, D, Abraham, SN, and MacLeod, AS. "IL-27 Facilitates Skin Wound Healing through Induction of Epidermal Proliferation and Host Defense." May 2017.

PMID
28132857
Full Text

Ratner, D, Orning, MPA, Proulx, MK, Wang, D, Gavrilin, MA, Wewers, MD, Alnemri, ES, Johnson, PF, Lee, B, Mecsas, J, Kayagaki, N, Goguen, JD, and Lien, E. "The Yersinia pestis Effector YopM Inhibits Pyrin Inflammasome Activation." PLoS pathogens 12, no. 12 (December 2, 2016): e1006035-.

PMID
27911947
Full Text

Akula, MK, Shi, M, Jiang, Z, Foster, CE, Miao, D, Li, AS, Zhang, X, Gavin, RM, Forde, SD, Germain, G, Carpenter, S, Rosadini, CV, Gritsman, K, Chae, JJ, Hampton, R, Silverman, N, Gravallese, EM, Kagan, JC, Fitzgerald, KA, Kastner, DL, Golenbock, DT, Bergo, MO, and Wang, D. "Control of the innate immune response by the mevalonate pathway." Nature immunology 17, no. 8 (August 2016): 922-929.

PMID
27270400
Full Text

Wang, D, Höing, S, Patterson, HC, Ahmad, UM, Rathinam, VAK, Rajewsky, K, Fitzgerald, KA, and Golenbock, DT. "Inflammation in Mice Ectopically Expressing Human Pyogenic Arthritis, Pyoderma Gangrenosum, and Acne (PAPA) Syndrome-associated PSTPIP1 A230T Mutant Proteins." Journal of Biological Chemistry 288, no. 7 (February 15, 2013): 4594-4601.

Full Text

Hsu, Y-MS, Zhang, Y, You, Y, Wang, D, Li, H, Duramad, O, Qin, X-F, Dong, C, and Lin, X. "The adaptor protein CARD9 is required for innate immune responses to intracellular pathogens." Nature Immunology 8, no. 2 (February 2007): 198-205.

Full Text

Wang, D. "3-Hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin)-induced 28-kDa interleukin-1ß interferes with mature IL-1ß signaling." The Journal of biological chemistry.

Scholars@Duke

Wang, D, and Lin, . "Bcl10 plays a critical role in NF-kappaB activation induced by G protein-coupled receptors."

Scholars@Duke

Wang, D. "Phosphorylation of CARMA1 plays a critical role in T Cell receptor-mediated NF-kappaB activation."

Scholars@Duke

Wang, D. "CD3/CD28 costimulation-induced NF-kappaB activation is mediated by recruitment of protein kinase C-theta, Bcl10, and IkappaB kinase beta to the immunological synapse through CARMA1."

Scholars@Duke

Wang, D. "A requirement for CARMA1 in TCR-induced NF-kappa B activation."

Scholars@Duke

Pages