Edward J. Usherwood, PhD
Professor of Microbiology and Immunology
Microbiology and Immunology
University of Cambridge, U.K., Ph.D., 1997
University of Cambridge, U.K., BA 1994
Dr. Usherwood received his B.A. in 1990 in Natural Sciences from the University of Cambridge, U.K. He continued his studies at the University of Cambridge and was awarded his Ph.D. from the Department of Pathology in 1994. From 1994 to 1997 Dr. Usherwood undertook postdoctoral research at the University of Edinburgh, U.K. then he moved to Memphis, TN for further postdoctoral work in the Department of Immunology at St. Jude's Children's Research Hospital. From 1999 to 2001 he held a position as a Research Assistant Member at The Trudeau Institute, NY. He came to Dartmouth in 2001 as an Assistant Professor, then was promoted to Associate Professor in 2007 and Full Professor in 2013.
Molecular and Cellular Biology Graduate Programs
Molecular Pathogenesis Program
Norris Cotton Cancer Center
Dartmouth Medical School
Borwell Research Building - HB7556
1 Medical Center Drive
Lebanon NH 03756
Determining factors necessary for memory T cell responses to optimize immunotherapy.
Our work determines the factors necessary for long-term survival of T cells to maintain their protective activity against both tumors and virus infections. While there is typically a large expansion of T cells early during an immune response, only a minority of these cells have the ability to survive long-term in the host. This prolonged survival is necessary for providing sustained protection against re-infection or recurrence of tumors. In fact, a major positive prognostic indicator for adoptive T cell therapies targeting cancer is the length of time that these T cells are sustained in the patient.
Our laboratory uses a variety of cutting-edge molecular techniques coupled with in vivo and in vitro models to understand the fundamental programming of memory T cell responses. These range from manipulation of transcriptional regulation, cell-extrinsic signaling and gene editing to metabolic reprogramming of T cells. We then devise methods to exploit this knowledge to design T cells that can better survive in the hostile environment of a tumor and enhance anti-tumor activity.
NCI R01 "Immune surveillance in murine gammaherpesvirus infection"
NIAID R01 "T cell function in murine gammaherpesvirus infection"
Immune Therapy Advanced Course (MCB graduate program)
MCB graduate program core course
Mitochondrial dysfunction triggers actin polymerization necessary for rapid glycolytic activation.
Resident memory CD8+ T cells in regional lymph nodes mediate immunity to metastatic melanoma.
Endometrial Cancer Suppresses CD8+ T Cell-Mediated Cytotoxicity in Postmenopausal Women.
Control of B Cell Lymphoma by Gammaherpesvirus-Induced Memory CD8 T Cells.
Zbtb20 Restrains CD8 T Cell Immunometabolism and Restricts Memory Differentiation and Antitumor Immunity.
CD8+ T Cells Require ITK-Mediated TCR Signaling for Migration to the Intestine.
Dissociating STAT4 and STAT5 Signaling Inhibitory Functions of SOCS3: Effects on CD8 T Cell Responses.
Neuropilin-1 Regulates the Secondary CD8 T Cell Response to Virus Infection.
Myeloid-specific Acat1 ablation attenuates inflammatory responses in macrophages, improves insulin sensitivity, and suppresses diet-induced obesity.
Cross-species conservation of episome maintenance provides a basis for in vivo investigation of Kaposi's sarcoma herpesvirus LANA.