Publications by authors named "Gabriella Reeder"
Precise targeting of large transgenes to T cells using homology-directed repair has been transformative for adoptive cell therapies and T cell biology. Delivery of DNA templates via adeno-associated virus (AAV) has greatly improved knockin efficiencies, but the tropism of current AAV serotypes restricts their use to human T cells employed in immunodeficient mouse models. To enable targeted knockins in murine T cells, we evolved Ark313, a synthetic AAV that exhibits high transduction efficiency in murine T cells.
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- Cancers can be very different from each other depending on where they start and their specific changes in genes.
- * A research project at UCSF looked at 364 individual tumors from 12 types of cancer to find common patterns in how the immune system interacts with these tumors.
- * The study found specific immune patterns (called archetypes) that can help doctors understand cancer better and figure out new ways to treat it.
The autoimmune regulator (Aire), a well-defined transcriptional regulator in the thymus, is also found in extrathymic Aire-expressing cells (eTACs) in the secondary lymphoid organs. eTACs are hematopoietic antigen-presenting cells and inducers of immune tolerance, but their precise identity has remained unclear. Here, we use single-cell multiomics, transgenic murine models, and functional approaches to define eTACs at the transcriptional, genomic, and proteomic level.
View Article and Find Full Text PDFIntratumoral T cells that might otherwise control tumors are often identified in an "exhausted" state, defined by specific epigenetic modifications and upregulation of genes such as CD38, cytotoxic T-lymphocyte-associated protein 4 (CTLA4), and programmed cell death 1 (PD1). Although the term might imply inactivity, there has been little study of this state at the phenotypic level in tumors to understand the extent of their incapacitation. Starting with the observation that T cells move more quickly through mouse tumors the longer they reside there and progress toward exhaustion, we developed a nonstimulatory, live-biopsy method for the real-time study of T cell behavior within individual patient tumors.
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- The study explores the differences between mild and severe COVID-19 by analyzing immune cell responses in patients using a specialized blood analysis technique.
- It finds that patients with mild COVID-19 show a strong expression of interferon-stimulated genes (ISGs), while those with severe disease lack these ISG-expressing cells despite having high levels of anti-SARS-CoV-2 antibodies.
- The research suggests that severe cases may be counterproductive, as the antibodies produced can inhibit the immune response critical for fighting the virus, pointing to potential targets for new treatments.
Article Synopsis
- Many COVID-19 patients experience a range of symptoms, from mild to severe, and this study seeks to understand the differences in disease pathology between these groups.
- Mild COVID-19 patients show a consistent pattern of interferon-stimulated gene (ISG) expression across blood cells, while severe patients lack these cells despite having high levels of antibodies against the virus.
- Severe patients produce antibodies that block the creation of ISG-expressing cells, highlighting a dysfunctional immune response that could be targeted for new treatments.
Article Synopsis
- The study examines the differences between mild and severe COVID-19 cases, highlighting how patients with mild cases show a coordinated immune response while severe cases lack this.
- Severe COVID-19 patients have high levels of antibodies against the virus but also produce antibodies that disrupt the immune response associated with milder cases.
- The researchers suggest that the aggressive antibody responses in severe cases may harm the immune system's effectiveness, indicating potential targets for new immunotherapy treatments.