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

Horkheimer, I, Quigley, M, Zhu, J, Huang, X, Chao, N, and Yang, Y. "Modulation of CD4(+)CD25(+)Foxp3(+) Regulatory T Cells in the Recipients Is Necessary for Enhancing Anti-Tumor Immunity Following Stem Cell Transplantation." May 2009.

Scholars@Duke

Zhu, J, Huang, X, and Yang, Y. "The TLR9-MyD88 Pathway Is Critical for Adaptive Immune Responses to AAV Vectors in Gene Therapy." May 2009.

Scholars@Duke

Huang, X, and Yang, Y. "Innate immune recognition of viruses and viral vectors." Hum Gene Ther 20, no. 4 (April 2009): 293-301. (Review)

PMID
19272012
Full Text

Quigley, M, Martinez, J, Huang, X, and Yang, Y. "A critical role for direct TLR2-MyD88 signaling in CD8 T-cell clonal expansion and memory formation following vaccinia viral infection." Blood 113, no. 10 (March 5, 2009): 2256-2264.

PMID
18948575
Full Text

Zhu, J, Huang, X, and Yang, Y. "A critical role for type I IFN-dependent NK cell activation in innate immune elimination of adenoviral vectors in vivo." Mol Ther 16, no. 7 (July 2008): 1300-1307.

PMID
18443600
Full Text

Quigley, M, Huang, X, and Yang, Y. "STAT1 signaling in CD8 T cells is required for their clonal expansion and memory formation following viral infection in vivo." J Immunol 180, no. 4 (February 15, 2008): 2158-2164.

PMID
18250422
Scholars@Duke

Martinez, J, Huang, X, and Yang, Y. "Direct action of type I IFN on NK cells is required for their activation in response to vaccinia viral infection in vivo." J Immunol 180, no. 3 (February 1, 2008): 1592-1597.

PMID
18209055
Scholars@Duke

Novy, P, Quigley, M, Huang, X, and Yang, Y. "CD4 T cells are required for CD8 T cell survival during both primary and memory recall responses." J Immunol 179, no. 12 (December 15, 2007): 8243-8251.

PMID
18056368
Scholars@Duke

Quigley, M, Huang, X, and Yang, Y. "Extent of stimulation controls the formation of memory CD8 T cells." J Immunol 179, no. 9 (November 1, 2007): 5768-5777.

PMID
17947649
Scholars@Duke

Zhu, J, Huang, X, and Yang, Y. "Innate immune response to adenoviral vectors is mediated by both Toll-like receptor-dependent and -independent pathways." J Virol 81, no. 7 (April 2007): 3170-3180.

PMID
17229689
Full Text

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