Kyle K. Payne, PhD, is an Assistant Professor of Medicine, Section of Cancer Immunotherapy, at the Robert Wood Johnson Medical School and is a Resident Member of the Rutgers Cancer Institute. Dr. Payne is a trained immuno-oncologist, where he has spent the first 10 years of his career focused on dissecting mechanisms immune suppression in the tumor microenvironment. During his PhD training, under the supervision of Dr. Masoud Manjili at Virginia Commonwealth University, Dr. Payne largely focused on targeting the immunosuppressive activity of myeloid-derived suppressor cells. He demonstrated that these cells could be functionally reprogrammed into immunostimulatory ‘antigen-presenting-like’ cells to promote antitumor T cell activity in breast cancer (J Immunol., 2011; Payne et al. Breast Cancer Res Treat, 2013; Payne et al., Kmieciak*, Basu*, Payne* et al. J Leukoc Biol., 2018), thereby unveiling key features of myeloid-derived suppressor cell biology.
Following the completion of his dissertation, Dr. Payne joined the laboratory of Dr. Jose Conejo-Garcia to pursue his postdoctoral training, first at the Wistar Institute/The University of Pennsylvania, and then at the H. Lee Moffitt Cancer Center. During this time, Dr. Payne investigated the mechanism of unrelenting expression of PD-1 on the surface of tumor-infiltrating T cells. He found that the genomic organizer, SATB1, functions as a repressor of PD-1 through orchestration of NuRD complexes within Pdcd1 regulatory regions. In contrast, tumor-derived TGF-β signaling was found to decrease SATB1 expression through SMAD occupancy of the Satb1 promoter, thus defining tumor microenvironmental TGF-β as a driver of PD-1 expression in ovarian tumor beds (Stephens*, Payne* et al. Immunity, 2017).
To complete his postdoctoral training, Dr. Payne subsequently identified butyrophilin 3A1 (BTN3A1) as a T cell regulator in ovarian cancer. Dr. Payne’s research unveiled that BTN3A1 is overexpressed in high-grade serous ovarian carcinoma, where it suppresses αβ T cells through an N-linked glycosylation CD45-dependent mechanism. In preclinical studies, Dr. Payne found that targeting this molecule with clinical-grade fully human antibodies released αβ T cells from BTN3A1-mediated suppression. Intriguing, these antibodies concurrently promoted BTN3A1-dependent activation of Vγ9Vδ2 T cells to acquire cytotoxic activity against tumor cells (Payne et al. Science, 2020), thus creating new therapeutic approaches for the management of ovarian cancer.
Building from collaborative efforts (Song et al. Nature, 2018), current work in the lab is focused on characterizing the impact of novel stress response mechanisms within malignant cells as well as infiltrating leukocytes. We have a particular interest in interrogating mechanisms of cellular adaptation and metabolic reprogramming elicited by the tumor microenvironment.
Dr. Payne is a member of the American Association of Immunologists (AAI), the Society for Immunotherapy of Cancer, and the American Association for Cancer Research. He has served as an ad hoc reviewer and invited guest editor for scientific journals. He is a former American Cancer Society Postdoctoral Fellow, a current V Foundation for Cancer Research V Scholar, an NCI K22 awardee, and an Ovarian Cancer Research Alliance Early Career Investigator. He has also received the Pershing Square Sohn Prize from the Pershing Square Sohn Cancer Research Alliance; awarded to exceptional young scientists in the greater New York City area (https://psscra.org/winners/kyle-k-payne-phd/).