Our lab's main purpose is to study how vaccines can be reformulated to achieve better immunity. One way is to exploit how immune responses are generated from natural infections. Toll-like receptors (TLRs) are the primary sensors that recognize foreign and "hidden self" antigens and transduce signals to activate the innate immune system. We know that activation of dendritic cells by TLR stimulation is a critical component bridging the innate immune system to the adaptive immune response. Thus, our studies involve using agonists for TLRs and examining how they may act as adjuvants to enhance vaccines. However, a paradigm of TLR agonists is that while they are potent activators of the innate immune system, they are poor inducers of T cell responses. My project examines how covalently linking the TLR agonist to protein antigen overcomes this limitation, resulting in efficient generation of both CD4 and CD8 T cell responses. In particular, I am interested in how protein-conjugated TLR agonists induce cross-priming of CD8 T cells as the CTL response is crucial in our ability to fight viral infection and tumor growth. Further studies are also in the works to address how this simple reformulation of TLR agonists into a co-delivery system with a protein enhances the efficacy of the vaccine.

 

 

Awards/Publications:

Cancer Research Institute Pre-doctoral Emphasis Pathway in Tumor Immunology Fellowship (2005, 2006, 2007)