Research in the Antony Rosen Lab investigates the mechanisms shared by the autoimmune rheumatic diseases such as lupus, myositis, rheumatoid arthritis, scleroderma and SjogrenÕs syndrome. We focus on the fate of autoantigens in target cells during various circumstances, such as viral infection, relevant immune effector pathways and exposure to ultraviolet radiation. Our recent research has sought to define the traits of autoantibodies that enable them to induce cellular or molecular dysfunction. We also work to better understand the mechanisms that form the striking connections between autoimmunity and cancer.
The Erika Darrah Lab is primarily interested in the mechanisms underlying the development and progression of autoimmunity in rheumatoid arthritis (RA), with a particular focus on the peptidyl arginine deiminase (PAD) enzymes. We’re focused on understanding the development of PAD4-activating autoantibodies over time and how they contribute to the development of erosive disease. Studies are underway to determine if the newly discovered antibody is mimicking a naturally occurring PAD4 binding partner and to identify potentially pro-inflammatory effects of citrullinated proteins on effector cells of the immune system.
Research in the laboratory of Felipe Andrade, M.D., Ph.D., focuses on the mechanisms of systemic autoimmune diseases, particularly as they relate to the role of cytotoxic granule proteases in autoimmunity and viral clearance, mechanisms of autoantigen citrullination and pathways that control immune effector functions in autoimmune diseases. We currently focus on two principal areas: (1) defining the mechanisms that generate citrullinated autoantigens in vivo in rheumatoid arthritis and (2) understanding the pathways that control the activity of the peptidylarginine deiminase (PAD) enzymes in human neutrophils.
The Pomerantz Laboratory studies the molecular machinery used by cells to interpret extracellular signals and transduce them to the nucleus to affect changes in gene expression. The accurate response to extracellular signals results in a cell's decision to proliferate, differentiate or die, and it's critical for normal development and physiology. The dysregulation of this machinery underlies the unwarranted expansion or destruction of cell numbers that occurs in human diseases like cancer, autoimmunity, hyperinflammatory states and neurodegenerative disease.
Current studies in the lab focus on signaling pathways that are important in innate immunity, adaptive immunity and cancer, with particular focus on pathways that regulate the activity of the pleiotropic transcription factor NF-kB.
The Konig Lab focuses on chimeric T cell- and antibody-based strategies for the treatment of autoimmune rheumatic diseases and cancer. A primary goal of the translational research program is the development of antigen-specific and personalized immunotherapies for autoimmune diseases, with the intent to achieve sustained disease remission and functional cure. The lab further aims to establish precision T cell-targeting therapies for the treatment of various autoimmune diseases. Applying these tools to immuno-oncology, the lab utilizes cellular engineering strategies to augment the cytotoxic killing of solid cancers by the immune system.
Research in the Thomas Grader-Beck Lab aims to understand the pathogenesis of systemic autoimmune diseases—particularly systemic lupus erythematosus (SLE) and Sjögren’s syndrome—by taking a translational approach. Autoantibodies (antibodies that target self-molecules) are believed to contribute significantly to the disease process. We are studying mechanisms that may make self-structures immunogenic. We theorize that certain post-translational antigen modifications, which can occur in infections or malignant transformation, result in the expression of neoepitopes that spread autoimmunity in the proper setting. The team has combined studies that employ a number of mouse strains, certain gene-deficient mice and human biological specimens.