Genetically modified immune cells are a new class of “living medicines” to treat human diseases, providing powerful complements to traditional drugs based on small molecules or antibodies.
To harness the immense potential offered by these new therapeutics, the Gladstone-UCSF Institute of Genomic Immunology combines emerging biomedical technologies at the intersection of human immunology, genomics, CRISPR genome engineering, computational biology, and synthetic biology.
This institute’s scientists deepen knowledge of how DNA sequences control cell functions in the human immune system. Their discoveries will enable the next generation of immunotherapies for cancer, autoimmune diseases, infectious diseases, and other inflammatory diseases.
This institute is the result of a close partnership between Gladstone Institutes and UC San Francisco (UCSF). With lab space both at Mission Bay and Parnassus, it creates a unified community across the two campuses and combines UCSF’s world-class immunology and planned cell therapy efforts with Gladstone’s expertise in the host-pathogen interface, iPS cells, computational biology, and CRISPR gene editing technologies.
“We want to create an ecosystem that brings experts together to think about transformative opportunities for how patients can be treated in the future.”
Current Research Projects
Genome Engineering Primary Human T Cells
Researchers developed a robust CRISPR/Cas9-based technology that enables genome editing in primary human T cells. This enables the investigation of how variations in the genome that increase risk of autoimmune disease control the function of these key immune cells
Chemical Inhibition of Pathogenic T Cell Circuitry
Th17 cells play a central role in autoimmune diseases. Researchers identified small molecules that inhibit a gene that controls the formation Th17 cells. The scientists are now investigating the potential of developing these molecules into drugs that could be used to suppress autoimmunity
Genetic and Epigenetic Fine-Mapping of Causal Autoimmune Disease Variants
Although many genome variants have been linked to increased risk of autoimmune disease, the mechanisms by which they cause immune dysfunction are generally unknown. Researchers are mapping the genome, epigenome, and transcriptome of immune cells to identify the function of these genome variants.