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The Haining Laboratory studies the molecular mechanisms that impair T cell function in cancer and chronic infections using cellular immunology, chemical biology, and functional genomics to understand the regulatory circuits that drive loss of function by exhausted T cells. We are interested in developing novel therapeutic approaches to rescue function in exhausted T cells.
In our studies of functional and dysfunctional exhausted CD8 T cells, we used transcriptional profiling of rare populations of virus-specific CD8 T cells from human blood to identify the molecular differences between effective and ineffective T-cell responses in HIV. These studies revealed a mechanism by which PD-1 coordinately upregulates a program of genes, including the transcription factor BATF, which impairs T-cell function. Using chemical screens to identify small molecules that reverse inhibition caused by the receptor PD-1, we are developing novel genetic and computational approaches to match active compounds to their target molecules.
We have also developed a novel strategy for in vivo testing of regulators of T cell function in which an inducible shRNA construct is transduced into hematopoietic stem cells using a lentiviral vector, enabling in vivo gene knockdown without subsequent manipulation. This approach is particularly valuable for studying key genes that control endogenous tumor immunity.
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