Christine Beeton is an immunologist with an interest in autoimmunity and inflammation. She received a Bachelor and a Master of Science in Biochemistry from the Faculté des Sciences de Luminy within the Université de la Mediterranée in Marseille, France. She joined Dr. Evelyne Béraud’s group for her PhD in Immunology and then moved to the University of California, Irvine, to join Dr. K. George Chandy’s group in the Department of Physiology and Biophysics as a Postdoctoral Fellow in 2001. She was promoted to Assistant Researcher in 2006 and joined the faculty of the Department of Molecular Physiology and Biophysics at Baylor College of Medicine in 2008. In 2010 she assumed the role of Academic Director of the Cytometry and Cell Sorting Core for the Dan L. Duncan Cancer Center at Baylor College of Medicine.
As a Graduate Student, Christine Beeton was the first to show the benefits of blocking Kv1.1 and Kv1.3 channels with the scorpion venom peptide kaliotoxin to prevent and treat adoptive acute experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. She went on showing, in collaboration with Drs. Chandy and Wulff, that encephalitogenic T lymphocytes express more Kv1.3 channels than naïve T lymphocytes do and that targeting Kv1.3 channels only with ShK-Dap22 was sufficient to treat this model of multiple sclerosis. As a Postdoctoral Fellow, she continued her collaborative work with Dr. Wulff who showed that terminally differentiated human CCR7- effector memory T (TEM) lymphocytes up-regulate Kv1.3 channels upon activation whereas CCR7+ naïve and central memory T (TCM) lymphocytes up-regulate KCa3.1 channels. She demonstrated a similar switch in potassium channel phenotype in rat, but not mouse, T lymphocytes. In collaboration with the groups of Drs. Nepom, Andrews, and Calabresi she showed that T lymphocyte isolated from the synovial fluid of patients with rheumatoid arthritis and from the cerebrospinal fluid of patients with multiple sclerosis express high numbers of Kv1.3 channels. Through collaborative work with the groups of Drs. Pennington and Norton, she developed a novel analog of ShK, ShK-186 (now known as dalazatide), as a highly potent and selective blocker of Kv1.3 channels. ShK-186 preferentially inhibits human and rat TEM lymphocytes in vitro and in vivo and treats animal models of delayed type hypersensitivity, multiple sclerosis, rheumatoid arthritis, and asthma without preventing the clearance of acute viral or bacterial infections. Drs. Chandy, Beeton, and Pennington are inventors of a world-wide patent on ShK-186 and related compounds. This patent was licensed to Kineta, Inc. for the development of a new class of immunomodulators for the treatment of autoimmune diseases. Phase 1a and 1b clinical trials in healthy volunteers have shown that ShK-196 is well tolerated.
The Beeton Lab is interested in all aspects of translational research surrounding autoimmune and other chronic inflammatory diseases. Our expertise ranges from the isolation and culture of primary human and rodent cells (lymphocytes, monocyte/macrophages, and other immune cells; fibroblast-like synoviocytes; myoblasts), functional assays ex vivo (proliferation, production and secretion of cytokines, chemokines, proteases, migration, invasion, cytotoxicity, and more) and in vivo (trafficking, production and secretion of cytokines, chemokines, proteases, and more), patch-clamp electrophysiology on excitable and non-excitable cells for identification of ion channels and pharmacology of novel ion channel modulators, and animal models of inflammatory diseases in rats and mice (active and adoptive delayed type hypersensitivity, active and adoptive acute experimental autoimmune encephalomyelitis, chronic-relapsing experimental autoimmune encephalomyelitis, collagen-induced arthritis, pristane-induced arthritis, and adjuvant-induced arthritis). Our current work revolves around two main topics: targeting potassium channels for the treatment of chronic diseases (multiple sclerosis, rheumatoid arthritis, and type 1 myotonic dystrophy) and using antioxidant nanomaterials for the treatment of T lymphocyte-mediated autoimmune diseases (multiple sclerosis and rheumatoid arthritis).