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Sheng Wei, M.D.
Associate Professor in the Interdisciplinary Oncology Program

Member-in-Residence of the Moffitt Cancer Center

E-mail: Sheng.Wei@moffitt.org
Phone: 813-745-3934

Training
M.D.: Tianjin Medical University, Tianjin, China.
Postdoctoral Fellow: Univ. of South Florida, Department of Medical Microbiology and Immunology.

Research Interests
Dr. Wei's laboratory is focused on elucidation of the signal pathway for activation of human neutrophil function by cytokines and bacterial products. He has made a key discovery that GM-CSF, IL-2 and LPS signal via src-kinase-related protein tyrosine kinase, Lyn, suggesting that Lyn is a common element in neutrophil activation. Lyn play a key role in neutrophil survival induced by GM-CSF. Use of anti-sense oligonucleotides to Lyn indicated that anti-sense Lyn could readily block GM-CSF induced neutrophil survival. Dr. Wei also identified a key role for MAP kinase in internalization and growth inhibition of C. albicans using the MAP kinase inhibitor and dominant negative MEK expression. An important discovery was that MAP kinase regulated the migration of proteolytic granules to the point of contact with C. albicans within neutrophil. Another focus is on the signals that control of Natural Killer Cell (NK) mediated tumor lysis. Analysis of signal molecules indicated that target ligation triggers a Ras-independent MAP kinase pathway that is required for lysis of the ligated tumor cells. Target engagement caused NK cells to rapidly activate MAP kinase and perforin/granzyme B polarization within NK cells towards the contacted target cells. The present effort is to further define downstream event from MAP kinase that could mediated functional activation of both human neutrophil and
NK cells
.

Search for publications by:   
This search will be conducted at the US National Library of Medicine (NLM) and PubMed.

Selected Publications
1. Wei, S., D. Gilvary, B. Corliss, S. Sebti, J. Sun, D. Straus, P. Leibson, J. Trapani, A. Hamilton, M. Weber and JY. Djeu. 2000. Direct tumor lysis by natural killer cells utilizes a Ras-independent MAPK signal pathway. J. Immunol. 165: 3811.

2. Wei, S., J. H. Liu, P. K. Burnette, A. M. Gamero, M. E. Elkabani, J. Y. Djeu. 2000. IL-2 modulates lyn and MAP protein kinase activity in human neutrophils. Immunobiology (in press).

3. K. Jiang, B. Zhong, D. Gilvary, B. Corliss, E. Hong-Geller, S. Wei and J.Y. Djeu. 2000. Pivotal role of PI-3 kinase in regulation of cytotoxicity of Natural Killer Cells. Nature Immunology (in press).

4. J. H., S. Wei, T. Lamy, P. K. Epling-Burnette, G. Starkebaum, J. Y. Djeu, T. P. Loughran. 2000. Chronic neutropenia mediated by FAS ligand. Blood 95:3219.

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Cancer Biology Ph.D. Program
H. Lee Moffitt Cancer Center, MRC-4 East
12902 Magnolia Drive
Tampa, Florida 33612
Phone: 813-745-6876
E-mail: CancerPHD@moffitt.org
Copyright © 2000 University of South Florida

 

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