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Julia Wu
e-mail address: srjwu@umich.edu

Mentor: Pavan Reddy, MD

 

Research Description

CD8+ cytotoxic T cells kill infected or transformed cells in an antigen-specific manner, playing an essential role in the adaptive immune response.  To develop cytotoxic capabilities, a naïve CD8+ T cell must be activated through an interaction between its T cell receptor (TCR) and an MHC I molecule on an antigen presenting cell (APC) loaded with the TCR’s cognate peptide.  This process is known as antigen presentation. Classically, peptide loaded on MHC I molecules is derived from endogenous protein.  However, there are instances where exogenously-derived peptide is presented on MHC I molecules to activate CD8+ T cells in a process called antigen crosspresentation.   Crosspresentation is critical for initiating a cytotoxic response against viruses that do not infect APCs and for the immune response to tumors.

Antigen crosspresentation is most efficiently performed by CD8+ dendritic cells (DCs), a subset of professional APCs. Little was known about the regulatory machinery of crosspresentation until the recent discovery that an ER-SNARE, Sec22b, is necessary for antigen crosspresentation by cultured bone marrow-derived DCs (BMDCs) but not for conventional antigen presentation by these cells. We are interested in interrogating the role of Sec22b in crosspresentation in viral infection models and in bone marrow transplantation.

 


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