Department of Medicine
University of Pittsburgh
Zengbiao Qi, PhD
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Research Assistant Professor Phone: 412-692-2211 |
Bio
Zengbiao Qi graduated from University of Oklahoma in Biochemistry in 2001. After graduation, he joined Immunobiology and Cancer programs in Oklahoma Medical Research Foundation in 2001 to study the effect of E proteins on the development and signaling of thymocytes. He joined PACCM as a Research Associate in Dr. Anuradha Ray’s group in 2004 and was promoted to Research Assistant Professor in 2007.
Academic and Research Interests
Dr. Qi is primarily interested in molecular mechanisms underlying tolerance induction in the lungs in response to allergens and pathogens. He uses various mouse models of inflammation employing allergens such as ovalbumin, a model antigen, as well as house dust mite, and infectious agents including bacteria and fungi to investigate the roles played by various immune modulators, such as TGF-b1, Notch1 and aryl hydrocarbon receptor (AHR) in the process of tolerance induction and inflammation.
Below are some examples of some of the findings in these areas.
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Figure 1: Increased frequency of Notch1-expressing cells under conditions of airway tolerance. When mice are subjected to a model of airway tolerance using aerosolized ovalbumin, the frequency of CD4+ T cells expressing Notch1 on their surface is more than that found when cells are isolated from mice with airway inflammation. |
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Figure 2. CD4+ T cells expressing membrane-bound TGF-b efficiently inhibit allergic airway inflammation which is compromised by blocking Notch1. Airway inflammation was induced by ovalbumin sensitization and aerosolized ovalbumin challenge (C). Tolerance was induced by repeated exposure to aerosolized ovalbumin (D). Airway inflammation was inhibited by transferring CD4+TGFb+ cells (E) but not CD4+TGFb- cells (F). The inhibition mediated by CD4+TGFb+cells was abolished by anti-Notch1 antibody (G) while an isotype control antibody did not show this effect. |
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Figure 3. TGFb1-mediated suppression of CD4+ T cell proliferation is inhibited by an inhibitor of g –secretase, which inhibits Notch1 activation. |
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Key Publications
Pillemer BB, Xu H, Oriss TB, Qi Z, Ray A. 2007. Deficient SOCS3 expression in CD4+CD25+FoxP3+ regulatory T cells and SOCS3-mediated suppression of Treg function. Eur J Immunol. 37:2082-2089
*Ostroukhova M, *Qi Z, Oriss TB, McCarthy BD, and Ray A. 2006. T Regulatory Cell-Mediated Immunosuppression Involves Activation of the Notch-HES1 Axis By Membrane-bound TGF-beta. J.Clin. Invest. 116: 996-1004 (*co-first authors ).
Qi Z, and Sun X, 2004. Hyper-response to T-cell receptor signaling and apoptosis of Id1 transgenic thymocytes. Mol.Cell. Biol. 24: 7313-7323.