Adam Courtney, Ph.D.

Assistant Professor of Pharmacology
Accepting Students?


Dr. Courtney earned his PhD in Biochemistry from the University of Wisconsin, Madison. During his graduate studies in the lab of Dr. Laura Kiessling, he investigated how antigen glycosylation can be sensed by B cells using an inhibitory lectin co-receptor that suppresses B cell signaling. Dr. Courtney completed his postdoctoral training in the lab of Dr. Arthur Weiss as a fellow of the Cancer Research Institute (CRI) at the University of California, San Francisco where he investigated the regulation of kinases and phosphatases in T cells. These studies revealed T cell antigen perception can be manipulated using genetic and drug-like interventions to target regulatory mechanisms that set a threshold for T cell activation. Dr. Courtney then joined the University of Michigan as an Assistant Professor in the Department of Pharmacology. Currently, his research group aims to understand T cell signaling pathways important for antigen recognition and to explore strategies that improve the capacity of T cells to recognize and eliminate cancer.

Research Description

The major focus of our research is T cell signaling pathways, their role in antigen recognition, and ultimately a T cell response. A T cell must remain inert to ubiquitous potential self-antigens, yet poised to respond when a foreign-antigen is encountered, such as those derived from pathogens or malignant cells. The capacity of a T cell to make these distinctions is impacted by T cell antigen receptor (TCR) signaling, and also other signaling inputs such as co-stimulation, that ultimately determine whether a T cell becomes activated or not. Our research seeks to determine how a T cell establishes a threshold for activation using signaling proteins, such as kinases and phosphatases. We interrogate these signaling proteins to determine how their regulation affects T cell activation using chemical and genetic tools. By leveraging these insights, one of our goals is to augment T cell-mediated anti-tumor responses against poorly immunogenic cancers by developing new strategies to alter antigen perception, overcome suppressive cues, and reverse T cell dysfunction.