Littman Laboratory: T Cell Development and Retroviral Pathogenesis

Yi (Benny) Yang
Postdoctoral Fellow of the Arthritis National Research Foundation
Ph.D. in Immunology, University of Connecticut, Farmington 2007
M.S. in Microbiology, Fudan University, Shanghai, China 2002
Yi.Yang@med.nyu.edu

I have been fascinated by the question of how various cellular and molecular components of the immune system are coordinated to mount precise and effective responses since my undergraduate studies. Following my heart, I chose to pursue a Ph.D. in immunology at the University of Connecticut where I received rigorous training and made an important discovery. I was interested in the immune responses mediated by gp96, an endoplasmic reticulum protein. To investigate its function in vivo, I developed a conditional knockout mouse of gp96. I demonstrated that gp96 was a master regulator of Toll-like receptors. I also elucidated the significance of macrophage-specific TLR responses in vivo. In the spring of 2008, I joined Dan Littman’s lab as a postdoctoral fellow to study the relationship between Th17 cells and disease. Th17 cells have been suggested to have a pathogenic role in multiple autoimmune diseases. However, the pathogenesis of Th17 cells in vivo is still not clear. I chose to focus on the pro-inflammatory cytokines and study their roles in pathogenic Th17 cell generation and autoimmune disease development. To this end, I am developing novel gene-targeted mice and studying their phenotypes.

Publications

N. Zhu, Y. Yang, S. Chen and S. Yu. 2000. A novel HLA-DRB4 allele (DRB4*NC) identified in the Chinese population. U.S. Chinese Journal of Microbiology and Immunology 2:42-45.

N. Zhu, N. Gao, Y. Wang, X. Wang and Y. Yang. 2004. Expression of the negative co-stimulatory ligand sCD152 in the yeast, Pichia pastoris, and its regulation of antigen specific immune responses. Intl. Immunopharmacol. 4:139-48.

M. A. Mihalyo, A. D. Doody, J. P. McAleer, E. C. Nowak, M. Long, Y. Yang and A. J. Adler. 2004. In vivo cyclophosphamide and IL-2 treatment impedes self-antigen-induced effector CD4 cell tolerization: implications for adoptive immunotherapy. J. Immunol. 172:5338-45.

Y. Yang and Z. Li. 2005. Roles of heat shock protein gp96 in the ER quality control: redundant or unique function? Mol. Cells 20:173-82.

B. Liu, Y. Yang, J. Dai, R. Medzhitov, M. A. Freudenberg, P. L. Zhang and Z. Li. 2006. TLR4 upregulation at protein or gene level is pathogenic for lupus-like autoimmune disease. J. Immunol. 177:6880-8.

Y. Yang, B. Liu, J. Dai, P. K. Srivastava, D. J. Zammit, L. Lefrancois and Z. Li. 2007. Heat shock protein gp96 is a master chaperone for toll-like receptors and is important in the innate function of macrophages. Immunity 26:215-26. (Previewed by Harding C.V. gp96 leads the way for Toll-like receptors. Immunity. 2007 26:141-3)