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Name: ZHANG Fuping
Title: Principal Investigator and Professor
Dept.: CAS Key Laboratory of Pathogenic Microbiology and Immunology
Tel: +86-10-64806110
E-mail: zhangfp@im.ac.cn
Add.: NO. 1 Beichen West Road, Chaoyang District, Beijing 100101, P.R.China
Prof. Fuping ZHANG received her Ph.D in Immunology at Institute of Virology, Chinese Academy of Preventive medicine. Before joining IMCAS, she was Trained as a Research Fellow in Vanderbilt University Medical Center, USA, and as IRTA fellow in National Institute of Allergy and Infectious Disease(NIAID), National Institute of Health(NIH) in U.S.A. The major focus of her lab research is study the transcription regulation mechanism of T cell subset specification, T cell immune response in autoimmune diseases and Th1/Th17 mediated immunity to infectious disease.

Research interests:

The major focus of research in her laboratory is the study of Transcriptional regulation of T lymphocytes differentiated into distinct functional subsets, the autoimmune T cell response and mechanism of Th1/Th17-mediated immunity to fungal and TB infection. These studies will help us to understand and manipulate the immune system, and to ultimately develop immune therapies for treating autoimmune and for eliminating infectious diseases. 

Their current interests are:

1. Transcriptional regulation of T lymphocytes differentiation into distinct functional subsets with diverse effector functions

CD4+ helper T cells are important producers of a range of cytokines, and it is through the differentiation of these cytokine producing T helper cell subsets that lead to the immune responses to eliminate a range of microbial pathogens. We have found several transcription factors that are involved in regulate different T cell subset differentiation previously. Therefore, the goal of this research program is to understand how these transcription factors regulate distinct CD4 T helper cell differentiation and to elucidate the mechanisms by which these transcription factors regulate the reciprocal relationship among certain T helper subset.

2. Mechanism of Th1/Th17-mediated immunity to Fungal and Tuberculosis bacteria infection

Host defense against pathogenic microorganisms requires extensive communication between innate and adaptive immunity. Signals from innate immune cells, induced by pathogens and inflammatory stimuli, drive naive CD4+ T cells to differentiate into different effector cell fates, including T helper 1 (Th1), Th2, and Th17 cells. By utilizing some of our KI/Conditional KO mice, another ongoing research effort in the laboratory is Study the mechanism by which certain component of fungus or mycobacteria stimulated Dendritic cell or macrophage lead to predominant Th17 mediated or Th1/Th17 mediated immune responses. Besides, we are also interested in how the products of differentiated T cells subsequently tailor immune responses to effectively eliminate intracellular and extracellular pathogens.

3. T helper cell in autoimmune diseases.

Cytokine producing CD4 T cells such as Th1 and Th17 have long been noted to drive autoimmune diseases such as inflammatory bowl disease (IBD) and multiple sclerosis (MS). The lab is interested in using of experimental models of both IBD (DSS colitis) and MS(EAE) to understand the complex cellular and molecular events governing mucosal inflammation and MS due to unbalanced Th1/Th17 immune responses. These project will led to new insights into the effector and regulatory mechanisms at play during inflammation and, to help the development of new approaches to the treatment of autoimmune diseases.


Awards & Honors:

Selected Publications and Books:

[1] Strober W, Zhang F, Kitani A, Fuss I, Fichtner-Feigl S. (2010) Proinflammatory cytokines underlying the inflammation of Crohn's disease. Curr Opin Gastroenterol. Jul; 26 (4):310-7.

[2] Meng, G., Zhang, F., Fuss, I., Kitani, A., and Strober, W. (2009) A Mutation in the Nlrp3 Gene Causing Inflammasome Hyperactivation Potentiates Th17 Cell-Dominant Immune Responses.  Immunity 30 860-874.

[3] Zhang, F., Meng, G. and Strober, W. (2008) Interactions among transcription factors Runx1, RORgt and Foxp3 regulate differentiation of interleukin17-producing T cells. Nature Immunology 9 :1297-1306.

[4] Zhang, F. and Boothby, M. (2006) Th1-specific Brg1 recruitment and remodeling of nucleosomes positioned at IFN-γ promoter is STAT4-dependent. Journal of Experimental Medicine 203:1493-1505.

[5] Corn, R.A., Aronica M.A., Zhang, F. et al. (2003) T cell-intrinsic requirement for NF-kappa B induction in post differentiation IFN-gamma production and clonal expansion in a Th1 response Journal of Immunology 171(4), 1816-1824.

[6] Zhang, F., Zhang, J., Zhou, W. et al. (2002) Expression of PrPc as His-fusion form in a baculovirus system and conversion of expressed PrP-sen to PrP-res in cell-free system. Virus Research 87 145-153.

[7] Zhang, F., Dong, X., Zhou, W. et al. (2002) Cloning and expression of S100 protein and establishment method to test S100 protein. Chinese Journal of Experiment medicine (1) 48-55.

[8] Zhang, F., Dong, X., Sun, X. et al. (2000) Preparation and primary application of 14-3-3 specific polyclonal antibody, Chinese Journal of Neurology, 33(5) 331-335.

[9] Zhang, F., Dong, X., Zhao, X. et al. (1999) cDNA cloning and expression in prokaryotic cells of neuron protein 14-3-3beta. Chinese Journal of Neurology 32(4): 230-233.

[10] Zhang, F., Deng. P., Men, Q.et al. (1998) The shift of sequential antibody response to ovine lentivirus in Xinjiang Merino sheep. Chinese Journal of Veterinary Medicine 24(3): 7-9.

[11] Zhang, F., Deng, P. Men, Q. et al. (1998) Isolation and identification of ovine Lentivirus (OvLv) from naturally infected Xinjiang Merino sheep.  Chinese Journal of Animal and Poultry Infectious Diseases. 20(2): 68-70.

Institute Of Microbiology Chinese Academy of Sciences
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