Judy Lieberman is a professor of pediatrics and adjunct professor of genetics at Harvard Medical School and an endowed chair in cellular and molecular medicine. Her lab studies cytotoxic T lymphocytes (CTL), key cells in the immune defense against viral infection and cancer, as well as molecular pathways activated by the granzymes, and how RNA interference (RNAi) regulates cell differentiation in health and disease states. We spoke to Judy about advice for early career researchers, how she first become interested in cytotoxic T lymphocytes, and key people who have provided mentorship across her career.
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| http://dx.doi.org/10.1084/jem.20241556 | DOI Listing |
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Small-molecule GSDMD agonism in tumors stimulates antitumor immunity without toxicity.
Cell
October 2024
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA. Electronic address:
Gasdermin-mediated inflammatory cell death (pyroptosis) can activate protective immunity in immunologically cold tumors. Here, we performed a high-throughput screen for compounds that could activate gasdermin D (GSDMD), which is expressed widely in tumors. We identified 6,7-dichloro-2-methylsulfonyl-3-N-tert-butylaminoquinoxaline (DMB) as a direct and selective GSDMD agonist that activates GSDMD pore formation and pyroptosis without cleaving GSDMD.
View Article and Find Full Text PDFTumor editing suppresses innate and adaptive antitumor immunity and is reversed by inhibiting DNA methylation.
Nat Immunol
October 2024
Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA.
Cancer cells edit gene expression to evade immunosurveillance. However, genome-wide studies of gene editing during early tumorigenesis are lacking. Here we used single-cell RNA sequencing in a breast cancer genetically engineered mouse model (GEMM) to identify edited genes without bias.
View Article and Find Full Text PDFInflammasome-independent pyroptosis.
Curr Opin Immunol
June 2024
Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
Gasdermins are membrane pore-forming proteins that cause pyroptosis, an inflammatory cell death in which cells burst and release cytokines, chemokines, and other host alarm signals, such as ATP and HMGB1, which recruit and activate immune cells at sites of infection and danger. There are five gasdermins in humans - gasdermins A to E. Pyroptosis was first described in myeloid cells and mucosal epithelia, which express gasdermin D and activate it when cytosolic sensors of invasive infection or tissue damage assemble into large macromolecular structures, called inflammasomes.
View Article and Find Full Text PDFPoking holes in the blood-brain barrier.
Immunity
June 2024
Program in Cellular and Molecular Medicine, Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
Bacterial lipopolysaccharide (LPS) is implicated in disrupting the blood-brain barrier (BBB). In a recent issue of Nature, Wei et al. now show that LPS activates the inflammatory caspases (4, 5, and 11) and gasdermin D (GSDMD) in brain endothelial cells, which triggers their pyroptotic cell death and disrupts the BBB.
View Article and Find Full Text PDFROS-dependent S-palmitoylation activates cleaved and intact gasdermin D.
Nature
June 2024
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Gasdermin D (GSDMD) is the common effector for cytokine secretion and pyroptosis downstream of inflammasome activation and was previously shown to form large transmembrane pores after cleavage by inflammatory caspases to generate the GSDMD N-terminal domain (GSDMD-NT). Here we report that GSDMD Cys191 is S-palmitoylated and that palmitoylation is required for pore formation. S-palmitoylation, which does not affect GSDMD cleavage, is augmented by mitochondria-generated reactive oxygen species (ROS).
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