Yersinia pseudotuberculosis is a close relative of Yersinia pestis, the etiologic agent of plague, and has been studied as a model for understanding mechanisms of Yersinia pathogenesis. All members of the genus Yersinia are highly lymphotropic and possess common virulence factors that interfere with cellular signaling and activation pathways. The YopJ protein causes cell death in macrophages as well as blocking cellular activation pathways. A second virulence factor, YopH, interferes with T and B lymphocyte functions. Although numerous studies have highlighted the key role played by dendritic cells (DCs) in stimulating and directing immune responses, little is currently known about the interactions between Yersinia and DCs and the ability of Yersinia to interfere with DC functions. This proposal outlines a plan to examine the impact of Yersinia infection on the ability of DCs to orchestrate adaptive immune responses. This work should lead to new understanding of the nature and mechanisms by which pathogens manipulate host immune responses, and potentially to new knowledge of host resistance mechanisms. This knowledge will be important in the development of future strategies against human pathogens.
| Brodsky, Igor E; Palm, Noah W; Sadanand, Saheli et al. (2010) A Yersinia effector protein promotes virulence by preventing inflammasome recognition of the type III secretion system. Cell Host Microbe 7:376-87 |
| Brodsky, Igor E; Medzhitov, Ruslan (2008) Reduced secretion of YopJ by Yersinia limits in vivo cell death but enhances bacterial virulence. PLoS Pathog 4:e1000067 |
| Wanner, K W; Anderson, A R; Trowell, S C et al. (2007) Female-biased expression of odourant receptor genes in the adult antennae of the silkworm, Bombyx mori. Insect Mol Biol 16:107-19 |
