Biopark 1 Rm 330
Education and Training
I recieved my doctoral degree (Dr.med/Ph.D.) in molecular immunology in the Hematology and Oncology Department of Hannover Medical School, Germany, where I received intensive training in molecular and cellular immunology and gained expertise on T cell immunity, with an emphasis on T cell immune tolerance on bone marrow/stem cell transplantation. My graduate thesis was published in Blood.
post-doctoral training: in T cell immunity at La Jolla Institute of Allergy and Immunology, San Diego, California and RIKEN center for Allergy and Immunology, Yokohama, Japan, where I mastered advanced molecular, cellular, and animal techniques. Later I received intensive training in the area of biochemistry of Toll-like receptor (TLR) signaling at Microbiology and Immunology Department, University of Maryland School of Medicine.
I have broad background in Cell Biology and Immunology, with specific training and expertise in Molecular Cell Biology and Biochemistry. As a senior research associate, my role is to investigate the molecular and cellular determinants of alloantigen specific tolerance using murine models of cardiac and pancreatic islet transplantation, specifically to determine the mechanisms drive regulatory T cell migration and immune suppression. My postdoctoral training includes understanding of the tolerant or none tolerant immune cells (such as T cells, dendritic cells and macrophages) in inflammatory diseases. Starting from my doctoral study in Germany, after then the research training at the La Jolla Institute of Allergy and Immunology and RIKEN center for Allergy and Immunology, until finish my postdoctoral training at the Microbiology and Immunology Department in University of Maryland School of Medicine, I mastered numerous advanced molecular and immune technologies including microarray technology, and gained expertise on animal model of diseases such as asthma, arthritis, sepsis, DSS-colitis, and skin transplantation. Since 2006, I intensively studied the post-translational modifications and interactions of key molecules of TLR4 signal complexes associated with endotoxin tolerance, and accomplished several peer-reviewed publications including one book chapter. Before I joined Dr. Bromberg’s lab, my recent work advanced on identifying potential therapeutic peptides, which specifically block TLR4 and TLR2 signaling. These results have been published in PNAS, J. Biol. Chem., J Immunol., and Cell Rep. After I received the Living Legacy Foundation (LLF) Transplantation Grant in 2016, My current LLF project in 2017 is focused on the regulation of immune cell migration during allograft transplantation.
Regulatory T cell lymphatic migration, and the lymphotoxin beta receptor (LTbR) signaling in endothelial cells (EC).
- Piao W, Xiong Y, Famulski K, Brinkman CC, Li L, Toney N, Wagner C, Saxena V, Simon T and Bromberg JS. (2018) Regulation of T cell afferent lymphatic migration by targeting LTβR-mediated non-classical NFκB signaling. Nat Commun. 9: 3020. PMID: 30069025. PMCID: PMC6070541.
- Piao W, Ru LW, Toshchakov VY. (2016). Differential adapter recruitment by TLR2 co-receptors. Pathog Dis., 74(5). PMID: 27150837.
- Piao W, Shirey KA, Ru LW, Lai W, Szmacinski H, Snyder GA, Sundberg EJ, Vogel SN, Toshchakov VY. (2015). A Decoy Peptide that Disrupts TIRAP Recruitment to TLRs Is Protective in a Murine Model of Influenza. Cell Rep., 11(12):1941-52. PMCID: PMC4490105.
- Piao W, Ru LW, Piepenbrink KH, Sundberg EJ, Vogel SN, Toshchakov VY. (2013). Recruitment of TLR adapter TRIF to TLR4 signaling complex is mediated by the second helical region of TRIF TIR domain. Proc Natl Acad Sci U S A., 110(47):19036-41 PMID: 24194546. PMCID: PMC3578136.
- Piao W, Vogel SN, Toshchakov VY. (2013). Inhibition of TLR4 Signaling by TRAM-Derived Decoy Peptides In Vitro and In Vivo. J. Immunol., 190:2263-2272. PMID: 23345333. PMCID: PMC3578136.
- Leah A. Couture, Piao W, Ru Lisa W., Vogel SN, Toshchakov VY. (2012). Targeting Toll-like Receptor (TLR) Signaling by Toll/Interleukin-1 Receptor (TIR) Domain-containing Adapter Protein/MyD88 Adapter-like (TIRAP/Mal)-derived Decoy Peptides. J Biol Chem., 287:24641-24648. PMID: 22648407.
- Medvedev AE, and Piao W. (2009). Analysis of functional role of TLR4 tyrosine phosphorylation. In: "Toll-Like Receptors", O'Neill L.A.J. and McCoy, C. (Eds). Methods Mol Biol., 517:145-67. PMID: 19378035.
- Medvedev AE, Piao W, Shoenfelt J, Rhee SH, Chen H, Basu S, Wahl LM, Fenton MJ, Vogel SN. (2007). Role of TLR4 tyrosine phosphorylation in signal transduction and endotoxin tolerance. J Biol Chem., 282:16042-53. PMCID: PMC2675888
- Piao W, Chen H, Song C, Marco Q, Wahl LM, Fitzgerald KA, Li LW, and Medvedev AE. (2009). Endotoxin tolerance dysregulates MyD88-dependent and TRIF-dependent signaling pathways and increases expression of negative regulators of TLR signaling. J Leukoc Biol., 86:863-75. PMCID: PMC2796624
- Piao W, Song C, Chen H, Wahl LM, Fitzgerald KA, O’Neill LA, Medvedev AE. (2008). Tyrosine phosphorylation of MyD88 Adapter-Like (Mal) is critical for Signal Transduction and Blocked in Endotoxin Tolerance. J Biol Chem., 283:3109-3119. PMCID: PMC2705934
My current research interest is focused on T cell migration and allograft tolerance. Our Lab (Dr. bromberg's Lab) found that regulatory T cells (Treg) that migrate from graft to lymph node (LN) via afferent lymphatics, but not from blood to LN via high endothelial venules (HEV), prolong graft survival. This indicates lymphatic endothelial cell (LEC) (rather than HEV) specifically modulate Treg function, and/or that sequential Treg migration from blood to the inflamed allograft and then to draining LN (dLN) is required for their optimal function. Additionally, we found that lymphotoxin is critical for Treg efferent lymphatice migration. My spesific interest is to regulate T cell migration by specifically targeting LTbR-mediated classical and non-classical NFkB signaling in LEC.
PI: Bromberg/Piao; Maryland Living Legacy Foundation; 3/15/16 – 3/14/17;
Control of lymphotoxin-dependent T cell migration and function through fine-tuning LTα1β2-LTβR signaling using LTβR-derived inhibitory peptides.
PI: Bromberg/Piao; Maryland Living Legacy Foundation; 5/30/16 – 5/29/18;
Modulation of inflammation and rejection by control of T cell migration through inhibition of LTα1β2-LTβR non-classical signaling using LTbR-derived inhibitory peptides