Yiping Yang, MD, PhD

Professor of Medicine
Professor of Immunology
Member of the Duke Cancer Institute
Campus mail 2019 Msrb-ii, 106 Research Drive, Durham, NC 27710
Phone (919) 668-0932
Email address yang0029@mc.duke.edu

The goal of Dr. Yang’s laboratory is to understand the molecular and cellular mechanisms leading to the generation of potent and long-lasting anti-tumor immunity, and to develop effective gene immunotherapeutic strategies for treating cancer. Furthermore, rational pre-clinical approaches will be tested in clinical trials in patients with Epstein-Barr virus (EBV)-related malignancies. Specifically, we focus on the following areas:

1. Innate Immunity to Viruses. Recombinant vaccinia virus and adenovirus have been developed as potent vaccine vehicles for treating cancer and infectious diseases. Recent studies have shown that the unique potency of these viruses lies in their effective activation of the innate immune system. How these viruses activate the innate immune system remains largely unknown. We have been interested in the role of pattern-recognition receptors including Toll-like receptors (TLRs)in innate immune recognition of these viruses as well as their signaling pathways. In addition, we are investigating the role of innate immune cells such as natural killer (NK) cells in innate and adaptive immune responses to these viruses. A full understanding of these processes will help us design effective vaccine strategies.

2. T Cell Memory. Eliciting long-lived memory T cell response is an ultimate goal of vaccination to provide long-term immunity against cancer. However, it is not clear what controls the formation of long-lived memory T cells. The understanding of mechanisms underlying memory T cell formation will provide important insights into the design of effective vaccines for treating cancer.

3. Regulatory T Cell Biology. Accumulating evidence has shown that the immunosuppressive CD4+CD25+Foxp3+ regulatory T cells (TReg) play a critical role in the suppression of anti-tumor immunity. However, little is known about how TReg suppress T cell activation in vivo. Delineation of mechanisms underlying TReg-mediated suppression in vivo will help develop strategies to overcome TReg-mediated suppression in favor of boosting anti-tumor immunity.

4. Immunotherapy for EBV-associated Malignancies. Clinically, EBV-associated malignancies such as Hodgkin’s lymphoma offer a unique model to explore antigen-defined immunotherapy approaches because EBV-derived tumor antigens are specific for tumor cells only. Using this clinical model, we will test the utility of rational strategies identified in our preclinical models.

Education and Training

  • Fellowship, Medical Oncology, Johns Hopkins University School of Medicine, 1999 - 2002
  • Residency, General Internal Medicine, University of Pennsylvania School of Medicine, 1996 - 1999
  • Ph.D., University of Michigan at Ann Arbor, 1993
  • M.D., Zhejiang University (China), 1985

Publications

Yang, Y, Su, Q, Grewal, IS, Schilz, R, Flavell, RA, and Wilson, JM. "Transient subversion of CD40 ligand function diminishes immune responses to adenovirus vectors in mouse liver and lung tissues." Journal of Virology 70, no. 9 (1996): 6370-6377.

PMID
8709265
Scholars@Duke

Jooss, K, Yang, Y, and Wilson, JM. "Cyclophosphamide diminishes inflammation and prolongs transgene expression following delivery of adenoviral vectors to mouse liver and lung." Human Gene Therapy 7, no. 13 (1996): 1555-1566.

PMID
8864756
Scholars@Duke

Yang, Y, Xiang, Z, Ertl, HCJ, and Wilson, JM. "Upregulation of class I major histocompatibility complex antigens by interferon γ is necessary for T-cell-mediated elimination of recombinant adenovirus-infected hepatocytes in vivo." Proceedings of the National Academy of Sciences of the United States of America 92, no. 16 (1995): 7257-7261.

PMID
7638177
Full Text

Yang, Y, and Wilson, JM. "Clearance of adenovirus-infected hepatocytes by MHC class I-restricted CD4+ CTLs in vivo." Journal of Immunology 155, no. 5 (1995): 2564-2570.

PMID
7650386
Scholars@Duke

Yang, Y, Trinchieri, G, and Wilson, JM. "Recombinant IL-12 prevents formation of blocking IgA antibodies to recombinant adenovirus and allows repeated gene therapy to mouse lung." Nature Medicine 1, no. 9 (1995): 890-893.

PMID
7585213
Scholars@Duke

Yang, Y, Li, Q, Ertl, HCJ, and Wilson, JM. "Cellular and humoral immune responses to viral antigens create barriers to lung-directed gene therapy with recombinant adenoviruses." Journal of Virology 69, no. 4 (1995): 2004-2015.

PMID
7884845
Scholars@Duke

Goldman, MJ, Yang, Y, and Wilson, JM. "Gene therapy in a xenograft model of cystic fibrosis lung corrects chloride transport more effectively than the sodium defect." Nature Genetics 9, no. 2 (1995): 126-131.

PMID
7719338
Scholars@Duke

Yang, Y, Nunes, FA, Berencsi, K, Furth, EE, Gönczöl, E, and Wilson, JM. "Cellular immunity to viral antigens limits E1-deleted adenoviruses for gene therapy." Proc Natl Acad Sci U S A 91, no. 10 (May 10, 1994): 4407-4411.

PMID
8183921
Scholars@Duke

Yang, Y, Engelhardt, JF, and Wilson, JM. "Ultrastructural localization of variant forms of cystic fibrosis transmembrane conductance regulator in human bronchial epithelial of xenografts." American journal of respiratory cell and molecular biology 11, no. 1 (1994): 7-15.

PMID
7517144
Scholars@Duke

Yang, Y, Nunes, FA, Berencsi, K, Gönczöl, E, Engelhardt, JF, and Wilson, JM. "Inactivation of E2a in recombinant adenoviruses improves the prospect for gene therapy in cystic fibrosis." Nature Genetics 7, no. 3 (1994): 362-369.

PMID
7522742
Full Text

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