Ph.D., Professor Principal Investigator,Molecular Immunology
Email: binli@sibs.ac.cn,biolibin@gmail.com
Education and Training
2001-2006:
Postdoctoral Fellow, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine
1996-2001:
Ph.D., College of Life Sciences, Peking University, Beijing, China
1992-1996:
B.S., Department of Biology, Anhui Normal University, Anhui, China
Academic Employments
2009- present:
Professor, Principal Investigator, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China
2006-2009:
Research Associate, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine
2002-2003:
Visiting research scholar, Sir William Dunn School of Pathology, University of Oxford, Oxford, UK
Professional Affiliations
Member of the American Association of Immunologists Associate member of the American Association for Cancer Research Associate member of the New York Academy of Sciences Guest Editor of Immunological Research in 2008
Awards
2007-2008 Sponsored Research Award, Nidus Laboratories, Inc. USA
Research Interests
Our research goal is to elucidate the cellular and molecular mechanisms regulating the immune response in health and disease including infectious diseases, autoimmune diseases and cancer. Currently, we are particularly interested in understanding the dynamic role of one subpopulation of T cells, namely CD4+CD25+FOXP3+ regulatory T cells (FOXP3+Tregs), in major human infectious diseases.
The level and activity of the forkhead family transcription factor FOXP3 determine the immune function of FOXP3+Tregs. At the beginning of infectious processes, FOXP3+Tregs may regulate effector immune cell responses and lead to failure to control infection. FOXP3+Tregs may also help to limit collateral tissue damage when the antiviral immune responses are too vigorous. Understanding the regulation of FOXP3 and the dynamic ensemble of FOXP3 with enzymatic cofactors in Tregs will provide therapeutic applications for major human viral infectious diseases including HIV, hepatitis B and C viruses.
Based on previous findings (Reviewed in Immunol Rev 212:99-113; Curr Opin Immunol 19(5):589-95; Cell Cycle 15;6(12):1432-6; and Immunology 123(1):17-9), we hypothesize that in both FOXP3+Tregs and FOXP3+ epithelial cells, 1) FOXP3 is highly regulated in a spatial and temporal manner in response to physiological signals during viral infection; 2) the function of FOXP3 is dependent on its posttranslational modification status; 3) the function of FOXP3 is also dependent on its dynamic ensemble with other binding partners, including several key transcription factors and enzymatic co-repressors and/or co-activators.
In order to test the hypothesis and elucidate the function of FOXP3+Tregs in infectious diseases, we will combine molecular, biochemical, structural, cellular and mouse genetic tools to work on the following projects: 1. To identify the binding partners, upstream regulators and downstream effectors of FOXP3 and analyze their function in modulating Treg activity in infectious diseases; 2. To study signal-dependent spatial and temporal regulation of FOXP3 level, activity and ensemble during infectious processes; 3. To examine activity-dependent post-translational modifications of FOXP3 and the functional consequences in response to various viral infection.
Selected publications (2006-2008)
1、 Samanta A*, Li B*, Song X, Bembas K, Zhang G, Katsumata M, Shen Y, Saouaf SJ, Hancock WW, Wang Q and Greene MI. (2008) TGF-beta and IL-6 signals modulate chromatin binding and promoter occupancy by acetylated FOXP3. THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. 105(37):14023-7. Epub 2008 Sep 8 (*co-first authors) 2、 Zhou Z, Song X, Li B*, and Greene MI*. (2008) FOXP3 and its partners: structural and biochemical insights into the regulation of FOXP3 activity. IMMUNOLOGIC RESEARCH. Epub 2008 July 15th DOI. 10.1007/s12026-008-8029-x. Review. (*co-corresponding authors). 3、 Zhou Z, Song X, Berezov A, Zhang G, Li Y, Zhang H, Murali R, Li B*, and Greene MI*. (2008) Human Glucocorticoid Induced TNF Receptor Ligand Regulates Its Signaling Activity Through Multiple Oligomerization States. THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. 105(14):5465-70. (*B.L. and M.I.G designed the research). 4、 Li B and Greene MI. (2008) FOXP3 Biochemistry in regulatory T cells. How diverse signals regulate suppression. IMMUNOLOGY. 123 (1), 17–19. The 50th anniversary issue, Feature in Tsup/Teff cells. Review. 5、 Li B, Samanta A, Song X, Iacono KT, Tao R, Shen Y, Riley JL, Hancock WW, Saouaf SJ, Greene MI. (2007) FOXP3 interactions with histone acetyltransferase and class II histone deacetylases are required for repression THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. 104 (11): 4571-4576 (Research Highlighted in Nature Immunology May 2007; 8 (5): 471) 6、 Li B, Samanta A, Song X, Iacono KT, Brennan P, Chatila TA, Roncador G, Banham AH, Riley JL, Wang Q, Shen Y, Saouaf SJ, Greene MI. (2007) FOXP3 is a homo-oligomer and a component of a supramolecular regulatory complex disabled in the human XLAAD/IPEX autoimmune syndrome. INTERNATIONAL IMMUNOLOGY 19 (7): 825–835. 7、 Li B and Greene MI. (2007) FOXP3 actively represses transcription by recruiting the HAT/HDAC complex. CELL CYCLE June 15, 2007; 6 (12): 1432-1436. Perspective. 8、 Li B, Saouaf SJ, Samanta A, Shen Y, Hancock WW and Greene MI. (2007) Biochemistry and therapeutic implications of understanding mechanisms underlying FOXP3 activity. CURRENT OPINION IN IMMUNOLOGY. 19(5):583-8. Epub 2007 Aug 20. Review. 9、 Li B, Samanta A, Song X, Furuuchi K, Iacono KT, Kennedy S, Katsumata M, Saouaf SJ, Greene MI. (2006) FOXP3 ensembles in T cell regulation. IMMUNOLOGICAL REVIEW. 2006 Aug; 212:99-113. Review. 10、 Li B, Song X, Samanta A, Bembas K, Brown A, Zhang G, Katsumata M, Shen Y, Saouaf SJ and Greene MI. (2008) FOXP3 biochemistry will lead to novel drug approaches for vaccines and diseases which lack suppressor T cells. The Immune Synapse as a Novel Target for Therapy, p147-154.? The series PROGRESS IN INFLAMMATION RESEACH. Book chapter. 11、 Li B*, Shen Y, Zhou Z, Song X, Bembas K, Zhao XY, Cai Z, Berezov A, Saouaf SJ, Zhang HT, Wang Q and Greene MI*. (2008) Epigenetic regulation of autoimmune diseases through deacetylase inhibition. THE EPIGENETICS OF AUTOIMMUNE DISEASE, edited by Prof. Moncef ZOUALI (Paris, France), John Wiley & Sons, Inc. Book chapter. In press. (*co-corresponding authors). 12、 Tao R, de Zoeten EF, Ozkaynak E, Chen C, Wang L, Porrett PM, Li B*, Turka LA, Olson EN*, Greene MI*, Wells AD, Hancock WW, (2007) Deacetylase inhibition promotes the generation and function of regulatory T cells. NATURE MEDICINE, 13(11):1299-307 (*B.L., M.I.G and E.N.O. were instrumental in early stages of the project; Research Highlighted in Science 26 October 2007:?Vol. 318. no. 5850, p. 537; also in Nature Reviews Drug Discovery 6, 958 December 2007). 13、 Tao R, de Zoeten EF, Ozkaynak E, Wang LQ, Li B, Greene MI, Wells AD and Hancock WW, (2007) Histone deacetylase inhibitors and transplantation. CURRENT OPINION IN IMMUNOLOGY. 19(5):589-595. Review. 14、 Brennan PJ, Saouaf SJ, Van Dyken S, Marth JD, Li B, Bhandoola A, Greene MI. (2006) Sialylation regulates peripheral tolerance in CD4+ T cells. INTERNATIONAL IMMUNOLOGY 18(5):627-35. 15、 Hirohashi Y, Wang Q, Liu Q, Li B, Du X, Zhang H, Furuuchi K, Masuda K, Sato N, Greene MI, (2006) Centrosomal proteins Nde1 and Su48 form a complex regulated by phosphorylation. ONCOGENE 25(45):6048-55.
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