Assistant Professor, Institute of Human Virology
725 W. Lombard Street
Education and Training
Department of Preventive Veterinary Medicine, Nanjing Agriculture University, Nanjing, China
Postdoctoral Fellow, Virology and Immunology
Department of Microbiology and Immunology, University of North Carolina, Chapel hill, NC
Dr. Guangming Li received his Ph.D. degree in Agronomy from Nanjing Agriculture University and did his post-doctoral training in Virology and Immunology at University of North Carolina at Chapel Hill (HIV-1 immune pathology) in Dr. Lishan Su's lab. From 2014 to 2020, Dr. Li continued his research in chronic viral infection induced immune pathology and immune therapy in the context of HIV infection as Research Associate. In October 2020, Dr. Li joined The Institute of Human Virology at UMSOM as Assistant Professor and continues his research to mechanistically understand HIV immune pathogenesis and develop novel therapeutic strategies for HIV-1 cure in either humanized mice in vivo or cell culture system in vitro. Dr. Li also works on developing novel anti-HIV CAR-T or CAR-NK cells therapy for treating chronic diseases including HIV-1 infection and cancer.
HIV-1, plasmacytoid dendritic cells, Immunopathology, immunotherapy, humanized mice, CAR-T
- Li, G., L. Cheng, and L. Su. 2021. Phenotypic and Functional Study of Human Plasmacytoid Dendritic Cells. Curr Protoc 1: e50.
- Li, G., Z. Zhang, N. Reszka-Blanco, F. Li, L. Chi, J. Ma, J. Jeffrey, L. Cheng, and L. Su. 2019. Specific Activation In Vivo of HIV-1 by a Bromodomain Inhibitor from Monocytic Cells in Humanized Mice under Antiretroviral Therapy. Virol. 93.
- Li, G., J. I. Nunoya, L. Cheng, N. Reszka-Blanco, L. C. Tsao, J. Jeffrey, and L. Su. 2017. Regulatory T Cells Contribute to HIV-1 Reservoir Persistence in CD4+ T Cells Through Cyclic Adenosine Monophosphate-Dependent Mechanisms in Humanized Mice In Vivo. Infect. Dis. 216: 1579-1591.
- Li, G., J. Zhao, L. Cheng, Q. Jiang, S. Kan, E. Qin, B. Tu, X. Zhang, L. Zhang, L. Su, and Z. Zhang. 2017. HIV-1 infection depletes human CD34+CD38- hematopoietic progenitor cells via pDC-dependent mechanisms. PLoS Pathog. 13: e1006505.
- Li, G., M. Cheng, J. Nunoya, L. Cheng, H. Guo, H. Yu, Y. J. Liu, L. Su, and L. Zhang. 2014. Plasmacytoid dendritic cells suppress HIV-1 replication but contribute to HIV-1 induced immunopathogenesis in humanized mice. PLoS Pathog. 10: e1004291.
Additional Publication Citations
- Cheng, L., H. Yu, J. A. Wrobel, G. Li, P. Liu, Z. Hu, X. N. Xu, and L. Su. 2020. Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-Seq. JCI Insight
- Zhao, J., L. Cheng, H. Wang, H. Yu, B. Tu, Q. Fu, G. Li, Q. Wang, Y. Sun, X. Zhang, Z. Liu, W. Chen, L. Zhang, L. Su, and Z. Zhang. 2018. Infection and depletion of CD4+ group-1 innate lymphoid cells by HIV-1 via type-I interferon pathway. PLoS Pathog. 14: e1006819.
- Cheng, L., Z. Zhang, G. Li, F. Li, L. Wang, L. Zhang, S. M. Zurawski, G. Zurawski, Y. Levy, and L. Su. 2017. Human innate responses and adjuvant activity of TLR ligands in vivo in mice reconstituted with a human immune system. Vaccine 35: 6143-6153.
- Cheng, L., H. Yu, G. Li, F. Li, J. Ma, J. Li, L. Chi, L. Zhang, and L. Su. 2017. Type I interferons suppress viral replication but contribute to T cell depletion and dysfunction during chronic HIV-1 infection. JCI Insight
- Cheng, L., J. Ma, J. Li, D. Li, G. Li, F. Li, Q. Zhang, H. Yu, F. Yasui, C. Ye, L. C. Tsao, Z. Hu, L. Su, and L. Zhang. 2017. Blocking type I interferon signaling enhances T cell recovery and reduces HIV-1 reservoirs. Clin. Invest. 127: 269-279
- Zhang, Z., L. Cheng, J. Zhao, G. Li, L. Zhang, W. Chen, W. Nie, N. J. Reszka-Blanco, F. S. Wang, and L. Su. 2015. Plasmacytoid dendritic cells promote HIV-1-induced group 3 innate lymphoid cell depletion. Clin. Invest. 125: 3692-3703.
- Whitehurst, C. B., G. Li, S. A. Montgomery, N. D. Montgomery, L. Su, and J. S. Pagano. 2015. Knockout of Epstein-Barr virus BPLF1 retards B-cell transformation and lymphoma formation in humanized mice. mBio 6: e01574-01515.
- Zhang, L., Q. Jiang, G. Li, J. Jeffrey, G. I. Kovalev, and L. Su. 2011. Efficient infection, activation, and impairment of pDCs in the BM and peripheral lymphoid organs during early HIV-1 infection in humanized rag2(-)/(-)gamma C(-)/(-) mice in vivo. Blood 117: 6184-6192.
- Liu, S. Y., R. Aliyari, K. Chikere, G. Li, M. D. Marsden, J. K. Smith, O. Pernet, H. Guo, R. Nusbaum, J. A. Zack, A. N. Freiberg, L. Su, B. Lee, and G. Cheng. 2013. Interferon-inducible cholesterol-25-hydroxylase broadly inhibits viral entry by production of 25-hydroxycholesterol. Immunity 38: 92-105.
- Novel HIV-1 therapeutic strategy in humanized mouse models: Our group at UMB is one of the top professionals to use human hematopoietic stem cells and human fetal lymphoid tissue engrafted humanized mouse models to study HIV-1 infection, pathogenesis and therapy. We were the first to study HIV-1 immuno-pathogenesis and therapy in the new generation of humanized Rag-C double knockout mouse or NSG model (DKO-hu and NSG-hu HSC mice). Since joining the faculty at UMB in year 2020 and working in Dr. Lishan Su’s lab, I have focused elucidating mechanisms of HIV-1 reservoir persistence and developing therapeutics for HIV infection in humanized mice in vivo.
- The HIV-1/pDC/IFN-I axis in HIV-1 infection, pathogenesis and cure: The precise role of pDC in HIV-1 pathogenesis is not clear. The conflicting reports in HIV-infected patients highlight the importance of studying the interaction between HIV-1 and pDC cells in relevant models. The human immune system engrafted humanized mouse model is a powerful tool to study human pDC development and function during HIV-1 infection in vivo. Most importantly, we have developed a critical anti-pDC mAb that efficiently depletes human pDC in vivo to investigate pDC-associated HVI-1 pathogenesis. Our studies show that HIV-1 can efficiently activate and productively infect human pDC in vivo. In addtion, pDC are the major (or only) cells producing type I interferons during HIV-1 infection, which contribute to suppressing HIV-1 replication in vivo. Most strikingly, depletion of pDC during HIV-1 infection resolves HIV pathogenesis in the presence of elevated levels of HIV infection. These findings suggest that pDC play a critical role in contributing to HIV pathogenesis and disease progression. Modulating pDC and IFN-I provides a novel approach to treating HIV-induced diseases.