This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. T lymphocytes (T-cells), an essential cellular component of the immune system, play a fundamental role in the elimination of invading micro-organisms. The cytotoxic T-cell (CTL) response towards viruses is directed towards class I Major Histocompatibility Complex (MHC-I) molecules complexed to viral peptide antigens (pMHC-I). However, CTLS are also responsible for less desirable immune outcomes such as transplant rejection, graft versus host disease and tissue destruction in autoimmune disease. These complexes are expressed on the surface of infected cells and are subsequently recognised specifically by clonally distributed ab T cell receptors (TcR) on CD8+ T-cells. Appropriately armed and activated CD8+ T-cells can eliminate infected cells and prevent viral replication. The formation of the specific TcR/pMHC-I complex is the central event of antigen recognition in the cellular immune response that activates the antigen-specific CTL. This proposal aims to examine the structures of defined TcR/pMHC complexes and their non-liganded components. All proposed research is presently funded by National Health & Medical Research Council (Australia) and the Australian Research Council. Hence proposed research has previously been peer-reviewed in depth.
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