Our laboratory focuses on the identification of immune alterations in systemic lupus erythematosus (SLE), a prototypic systemic autoimmune disease. We mainly work on specific human immune cell populations, including, NK cells T follicular helper (TFH) cells and B cells. We routinely use modern cellular biology techniques (single cell flow and mass cytometry, analysis of the metabolism of immune cells, single-cell-RNA-sequencing, quantitative proteomic analysis, confocal microscopy, transmission electron microscopy…) in combination with bioinformatics to identify SLE immune cells alterations.
Autophagy is a major catabolic pathway in the cells, which constantly delivers cytoplasmic constituents and organelles to the lysosomal compartment for degradation. During this process, a double membrane vesicle the so-called, autophagosome is formed, sequestering (selectively or not), a cytosolic cargo, and then fusing with late endosomes and lysosomes. The formation and function of autophagosomes requires the protein products of 35 autophagy genes (Atgs) some of them are also essential for a non-canonical form of autophagy the so-called LC3-associated phagocytosis (LAP).
Since the outbreak of the SARS-CoV-2 epidemic in 2020, we have drawn on the experience gained to find new methods and make improvement to existing ones. With the focus on providing efficient techniques to measure SARs-CoV-2 specific antibody response, we developed a multiplex assay using the Luminex technique to evaluate the presence of antibodies as well as their capacity of neutralization.
The main interest of the LLI is to define the cellular and molecular bases of immunodeficiency diseases and to develop new therapeutic approaches for these disorders. Through research and clinical activity in this field, we have been able to contribute to the discovery of the genes responsible for immunodeficiencies (e.g. JAK3-deficiency and reticular dysgenesis) and to define important clinical features of these disorders, as well as some of the immunological mechanisms leading to disease in affected patients, with particular interest to the Wiskott-Aldrich syndrome (WAS) and adenosine deaminase deficiency (ADA-SCID).
The antibody discovery platform established by Dr. Craig Fenwick and Professor Giuseppe Pantaleo in the Division of Immunology and Allergy at the CHUV has a research focus to discover novel fully human antibodies to target established and emerging infectious diseases. Through the isolation of virus specific B cells in post-infected or vaccinated donors, the platform is able to screen through thousands of B cell clones to discover the rare antibodies that have the best neutralizing potency and bind regions of the viral protein that are highly conserved and less likely to mutate.
Dr. Obeid has made numerous outstanding clinical research contributions that have led to significant improvements in the understanding of the pathogenesis mechanisms of immunotoxicities and the treatment of immune-related adverse events (irAEs), leading to the establishment of new imaging strategies for ICI-related myocarditis and the implementation of new personalized treatment approaches for refractory toxicities.
The Laboratory of Molecular Immunology and Vaccinology (LMIV) conducts basic and translational studies related to human humoral immune system function in healthy and pathological conditions. Our lab's principal efforts focus on mechanistic, structural and functional studies of protein complexes, with emphasis on the development of novel vaccines and identification of site of vulnerability of pathogens. To gain detail description of these processes and to characterize novel therapeutic targets, we integrate cutting-edge structural biology methods from cryo-electron microscopy, molecular biology and biochemical techniques, computational modeling and functional immunoassays. Our efforts are done in close collaboration with several groups within the Lemanic arc.
The immune-monitoring platform, developed by Dr. Craig Fenwick and Professor Giuseppe Pantaleo, has as its principal goals to identify the immunological profiles associated with different infectious agents, disease states, cancers, and induced by registered and experimental vaccines. Profiling consists of phenotypic identification, characterization of cellular activation states, cell fate evaluation, functionality, phosphosignaling and transcriptomic characterization of immune cells and tissues. The platform achieves its goals through the implementation of established and emerging analysis technologies for phenotypic, functional and genetic characterization of immune cells and through quantitative analysis of serum cytokine and chemokine levels as markers of inflammation, infection and disease.
My laboratory focuses primarily on the immuno-virological mechanisms associated with human immunodeficiency virus (HIV) pathogenesis and viral persistence.
The hallmark of untreated HIV infection is a gradual loss of CD4 T cells, with progressive impairment of the immune system that ultimately leads to acquired immunodeficiency syndrome (AIDS). In this context, one of our goals is to study the immuno-virological mechanisms associated with T-cell functional impairment.
Our laboratory focuses on the development of cell-based therapies for non-oncological diseases. We are primarily interested on precision gene editing and redirecting human effector and regulatory T cells specificities using CRISPR-Cas9-based technologies.
The overall aim of the research in our laboratory is to characterize theunderlying immune mechanisms of allograft rejection, in order to define novel therapeutic strategies that would promote graft survival. We have therefore developed experimental transplantation (Tx) models, with a particular interest in the biology of regulatory T cells and their role in the induction of Tx tolerance.
Primarily devoted to the research in Multiple Sclerosis (MS), our Laboratory studies the interaction between the immune response - with a focus on CD8+ T cells - and environmental factors. In particular, we have investigated the mechanism by which Epstein-Barr virus (EBV) might be implicated in the pathogenesis of MS. We have found that EBV-specific CD8+ T cells are dysregulated in the blood and the cerebrospinal fluid (CSF) of MS patients.