A5046717979- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immune Cell Function and Interaction
- CAR-T cell therapy research
- Adenosine and Purinergic Signaling
- T-cell and B-cell Immunology
- Phagocytosis and Immune Regulation
- Cytomegalovirus and herpesvirus research
- Inflammasome and immune disorders
- Immune Response and Inflammation
- Immune cells in cancer
- Multiple Myeloma Research and Treatments
- Epigenetics and DNA Methylation
- Immunodeficiency and Autoimmune Disorders
- Genetic and Kidney Cyst Diseases
Imperial College London
2021-2023
University of Cambridge
2019-2021
Mitochondria drive CTLs’ killer instinct Cytotoxic T lymphocytes (CTLs) can terminate both virally infected cells and cancer by secreting cytolytic proteins such as perforin granzyme B. CTLs are particularly effective because they sequentially kill multiple targets in a process called serial killing. Lisci et al . have identified mitochondria important regulators of CTL Mice lacking the deubiquitinase USP30 acutely depleted mitochondria, these reduced killing ability but normal motility,...
CD8 cytotoxic T lymphocytes (CTLs) rely on rapid reorganization of the branched F-actin network to drive polarized secretion lytic granules, initiating target cell death during adaptive immune response. Branched is generated by nucleation factor actin-related protein 2/3 (Arp2/3) complex. Patients with mutations in complex 1B (ARPC1B) subunit Arp2/3 show combined immunodeficiency, symptoms dysregulation, including recurrent viral infections and reduced CD8+ count. Here, we that loss ARPC1B...
Cytotoxic T lymphocytes (CTLs) are highly effective serial killers capable of destroying virally infected and cancerous targets by polarized release from secretory lysosomes. Upon target contact, the CTL centrosome rapidly moves to immunological synapse, focusing microtubule-directed at this point [1-3]. Striking similarities have been noted between polarization synapse basal body docking during ciliogenesis [1, 4-8], suggesting that centrosomes might dock with plasma membrane killing, in a...
EROS (essential for reactive oxygen species) protein is indispensable expression of gp91 phox , the catalytic core phagocyte NADPH oxidase. deficiency in humans a novel cause severe immunodeficiency, chronic granulomatous disease, but its mechanism action was unknown until now. We elucidate role EROS, showing it acts at earliest stages maturation. It binds immature 58 kDa directly, preventing degradation and allowing glycosylation via oligosaccharyltransferase machinery incorporation heme...
Abstract EROS (Essential for Reactive Oxygen Species) protein is indispensable expression of gp91 phox , the catalytic core phagocyte NADPH oxidase. deficiency in humans a novel cause severe immunodeficiency, chronic granulomatous disease (CGD), but its mechanism action was unknown until now. We elucidate role EROS, showing it acts at earliest stages maturation. It binds immature 58kDa directly, preventing degradation and allowing glycosylation via oligosaccharyltransferase (OST) machinery...
Abstract Chronic Granulomatous Disease (CGD) is an inborn error of immunity characterised by opportunistic infection and sterile granulomatous inflammation. CGD caused a failure reactive oxygen species (ROS) production the phagocyte NADPH oxidase. Mutations in genes encoding oxidase subunits cause CGD. We others have described novel form (CGD5) secondary to lack EROS ( CYBC1 ), highly selective chaperone for gp91 phox . EROS-deficient cells express minimal levels its binding partner p22 ,...
CD8 cytotoxic T lymphocytes (CTLs) rely on rapid reorganization of the branched F-actin network to drive polarized secretion lytic granules, initiating target cell death during adaptive immune response. Branched is generated by nucleation factor actin-related protein 2/3 (Arp2/3) complex. Patients with mutations in complex 1B (ARPC1B) subunit Arp2/3 show combined immunodeficiency, symptoms dysregulation, including recurrent viral infections and reduced CD8+ count. Here, we that loss ARPC1B...