Center Events

Imtiaz A. Khan, PhD - Professor of Microbiology, Immunology, and Tropical Medicine, George Washington School of Medicine & Health Sciences

Toxoplasma gondii is a major food-borne illness that causes severe disease in humans, especially newborns and immunocompromised individuals. CD8 T cell immunity is critical for keeping chronic infection under control, During later phases of chronic infection, CD8+ T cells develop exhaustion which compromises long-term immunity against the parasite, causing reactivation of latent infection. Maintenance of functional memory CD8 population is highly essential for host survival and it is critical to understand the mechanism by which this response can be achieved. Data from our laboratory demonstrates that CD8 T cell response is comprised of heterogenous population including one effector and three memory populations. The process is complex and individual contribution of memory subsets in the generation of effector response need to be studied.

 Sep 09, 2024 @ 12:00 p.m.
 Medical Center | Upper Aud. (3-7619)

Chenghao Wang - Graduate Student

Toxoplasma is a common intracellular parasite that can infect almost all nucleated cells. Innate immune recognition of this pathogen leads to the production of chemokines and IL-12, which are crucial for host resistance to the parasite. We have previously defined the key steps involved in T. gondii recognition in the mouse system and identified TLR11 as a major innate immune sensor that recognizes T. gondii profilin and triggers a potent MyD88-dependent IL-12 response essential for host resistance.

Additionally, we recently revealed that the production of CCL2 by mouse and human cells is central to regulating immunity to T. gondii. We and others have shown that this response can be induced via TLR11-dependent and independent mechanisms, with the TLR11-independent release of the human alarmin S100A11 contributing to CCL2 production. In my work, I identified that, in addition to proteins, the release of lipids from T. gondii-infected human cells plays a role in the induction of CCL2 by monocytes. Furthermore, different T. gondii virulence factors may influence the parasite's recognition by human cells and the lipid-mediated induction of CCL2. The current work is focused on the molecular mechanisms responsible for the release of lipids during T. gondii infection of human cells.

 Sep 12, 2024 @ 12:00 p.m.
 Medical Center | K307 (3-6408)

Yuchang Liu - Graduate Student

Antibiotic resistance has been an increasing global health issue, and the spreading of antibiotic resistance will lead to the emergence of multi-drug resistance bacteria. While conjugation is one of the most important ways of spreading antibiotic resistance, separate plasmid transfer events always exhibit different efficiencies. Right now, the literature consensus believes that recipient strains will not play a large role in dictating conjugation efficiencies, but all the previous studies just used KO or mutant libraries of the same parent strain, which can only induce low genetic diversity. Hence, there is a gap in our mechanistic understanding of recipient-specific features that impact conjugation efficiency. However, due to the genetic differences between different strains, they will probably build up different conditions and barriers for the plasmids, and thus show different abilities to receive the plasmids. In addition, we collected more than 30 drug-susceptible Klebsiella pneumoniae isolates, and found their abilities to receive plasmids are significantly different. We aim to explore the factors that determine an optimal plasmid recipient in the genetic aspect. Currently, we have found several potential gene clusters that might contribute to the high conjugation efficiency phenotype through a functional genomic screen. We also have verified that the insertion of some of these potential genes will make a difference in the conjugation efficiency. In the future, we will also try to find out the genes that contribute to the low conjugation efficiency.

 Sep 12, 2024 @ 12:30 p.m.
 Medical Center | K307 (3-6408)