• Researcher Profile

    W. Nicholas Haining, BM, BCh

     
    W. Nicholas Haining, BM, BCh
     
    Physician

    Adjunct, Department of Immunology and Virology
    Assistant Professor, Pediatric Oncology
    Associate Professor of Pediatrics, Harvard Medical School
    Associate Member, Broad Institute of MIT and Harvard

    Center/Program

    Pediatric Stem Cell Transplant

    Office phone: 617-632-5293
    Fax: 617-632-4410
    Email: nicholas_haining@dfci.harvard.edu
    Website: Haining Lab Website

    Preferred contact method: email

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    Research Department

    Pediatric Oncology

    Interests

    Biological therapy/immunotherapy, Hematopoietic stem cell transplantation

    Area of Research

    Molecular mechanisms that impair T cell function in cancer and chronic infections


    Dana-Farber Cancer Institute
    450 Brookline Avenue
    Dana 640D
    Boston, MA 02215

    Research

    Molecular mechanisms that impair T cell function in cancer and chronic infections

    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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