OUR TEAM
Kebin Liu, Ph.D.
Founder and Administrative Officer
Dr. Liu is an expert in immunobiology and immunotherapy. He has decades of expertise in research of target-immune system interactions for the development of molecular mechanism-based therapies to boost the immune system to fight diseases, such as cancer and inflammatory diseases. In the tumor immunobiology field, Dr. Liu’s research focuses on the molecular mechanism underlying tumor cell acquisition of resistance to immune attack and resultant immune escape, with a particular interest in epigenetic regulation of genes involved in tumor cell survival mechanisms. In the tumor immunotherapy field, Dr. Liu has been in the frontline in elucidating the molecular mechanisms underlying tumor-induced immune suppression with a particular interest in myeloid-derived suppressor cells (MDSCs). The rationale is that if tumor cells are resistant to immune cell (e.g., T cells) cytotoxicity and/or can mount an immune suppressive response, then the cytotoxic T cells (CTLs) are not going to be able to kill the tumor cells regardless how potent these T cells are. Our aim is thus to develop targeted therapies to disarm tumor cell defense mechanisms (survival and immune suppression) and to arm T cells to achieve maximal efficacy in cancer immunotherapy.
Dr. Liu has recently expanded to the new research area in therapy for COVID-19. The major focus is two fold: first, he is interested in the underlying mechanism of NF-ҝB-mediated cytokine release syndrome in COVID-19 pathogenesis; and second, he and CheMedImmune are developing antagonists and blockade antibodies based on the interaction between SARS-2-S and ACE2 to block SARS-CoV-2 infection of human cells.
Professional Membership:
American Association for Cancer Research
American Association of Immunologists
Priscilla S. Redd, PhD
Senior Scientist
Dr. Redd has a Ph.D. degree in Biochemistry and Cancer Biology and postdoctoral training in T cell immunology and tumor immunotherapy. Dr. Redd has made significant contributions in determining the functions of and mechanism underlying NF-ҝB regulation of gene expression in tumor cells, myeloid cells, and T cells. Dr. Redd determined that PD-1 expression is mediated by epigenetic as well as transcriptional regulation. Specifically, she discovered that H3K4me3 and the NF-ҝB p50 homodimer upregulate PD-1 expression in T cells. To translate laboratory findings to cancer immunotherapy, Dr. Redd has been working on developing PD-1 small molecule antagonists to block the interaction of PD-1 and PD-L1 so that T cells can keep their effector function to target tumor cells. At the same time, Dr. Redd has been studying another immune suppressive mechanism by which tumor cells bypass immune surveillance through osteopontin (OPN) overproduction. OPN is expressed and secreted by tumor cells and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. OPN then functions to suppress CTL activation. Dr. Redd is the Principal Investigator of a NCI SBIR grant entitled “OPN neutralization monoclonal antibody 100G2 for human pancreatic cancer immunotherapy.” The goal is to develop a humanized OPN monoclonal antibody to block OPN-induced immune suppression for human colorectal and pancreatic cancer immunotherapy.
Professional Membership:
American Association for Cancer Research
American Association of Immunologists
John D. Klement. Ph.D (MD-Ph.D Student)
Scientist
John obtained his BS degree from Yale University with a major in Biochemistry and research training in immunology. He is currently in the Medical College of Georgia MD-Ph.D program. He completed 3 years of Medical School and just completed his Ph.D degree with distinction. John is expected to obtain his MD degree in two years. John’s major contribution to science is the discovery of OPN as a new immune checkpoint. OPN is a secreted protein that is known to be involved in cancer and other human diseases. The elevated OPN production has been linked to poor prognosis in human cancer, especially colorectal cancer. John discovered for the first time that OPN functions as an immune checkpoint and negatively regulates T cell activation to promote tumor immune evasion. He further determined that tumor cells and myeloid-derived suppressor cells (MDSCs) are the two major sources of OPN in the tumor microenvironment. Based on these findings, four OPN neutralization monoclonal antibodies have been developed. These four OPN monoclonal antibodies have potent efficacy in blocking OPN function in the suppression of T cell activation ex vivo. Preliminary studies in preclinical immune competent tumor-bearing mice indicate that these OPN monoclonal antibodies are effective in suppression of tumor growth in vivo. He is actively involved in translating his discovery and OPN monoclonal antibodies to human colorectal and pancreatic cancer immunotherapy.
Professional Membership:
American Association for Cancer Research
American Association of Immunologists
