Ellen Heber-Katz

Professor at Lankenau Institute for Medical Research (LIMR)

Dr. Ellen Heber-Katz is a Professor at the Lankenau Institute of Medical Research. She has made important discoveries in both immunology and in regenerative medicine. For her PhD (UPenn) she demonstrated that single T-cell subsets could respond to both histocompatibility antigens and environmental antigens establishing the unity of these two branches of the immune response. This theme continued as a postdoctoral fellow at the NIH with the first functional evidence for the T cell–antigen-MHC-Ia tri-molecular complex anticipating the crystal structure. At the Wistar Institute as an Assistant Professor, she developed the first vaccine capable of eliciting a purely T cell response which was fully protective against a lethal challenge of Herpes Simplex Virus (HSV) in the absence of antibodies, and patented a generic structure for a purely T-cell activating vaccine. That T-cells alone (in the absence of a detectable antibody response) could confer protection against a lethal viral challenge was completely outside of mainstream thinking and totally ignored at the time (mid-1980s). Today, this is recognized as a critical vaccine concept. In the area of autoimmunity, she showed that pathogenic T cell responses used a very limited set of shared T-cell receptors. This was an unexpected result (and highly controversial at the time) but since then it has been shown to be the case for multiple autoimmune diseases and has recently been supported by genetic mapping studies. During her studies of autoimmune disease, she discovered that the MRL mouse, generally used for lupus studies, was capable of a profound regenerative response. This strain had been used for over 30 yrs in many mouse studies and this medically significant phenotype had previously not been noticed. Over the past 14 years, the Heber-Katz laboratory has explored the genetic, molecular, cellular, and physiological expression of this regenerative capacity. She has shown that this resident mammalian regenerative capacity (presumed to have been lost in evolution) could be unleashed by the suppression of a single gene, p21, establishing a new template for regenerative medicine as well as defining a role for a glycolytic metabolism in regeneration. Most recently, she identified HIF-1 as the key molecule in the regenerative response and together with the Messersmith Laboratory at Berkekley, a drug and delivery system was shown to replicate MRL-like regeneration in multiple systems.