Jason G. Cyster

Biosketch

Dr. Cyster is Professor of Microbiology and Immunology at the University of California, San Francisco. He graduated from the University of Western Australia with a BSc Honors degree in Biochemistry and Microbiology and completed a DPhil in Immunology at the University of Oxford in the laboratory of Alan Williams. He was a postdoctoral fellow in immunology at Stanford University with Christopher Goodnow and he joined the faculty at UCSF in 1995. Dr. Cyster is internationally recognized for defining how lymphoid microenvironments are organized to support adaptive immunity. His lab played a key role in the discovery of lymphoid tissue chemokines and established the concept that chemokines continuously guide cells to supportive niches. Dr. Cyster’s group led the way in defining how cells exit from lymphoid organs, a process essential for immune function. His team established the egress-promoting role of sphingosine-1-phosphate and identified the mechanism of action of key egress regulators. He has been a leader in applying two-photon microscopy to unraveling antigen-encounter and immune cell migration dynamics. He received the 2005 AAI BD Biosciences Investigator Award in Recognition of Outstanding Contributions in Immunology and the 2018 AAI Biolegend Herzenberg Award for outstanding contributions in B cell biology.

Research Interests

My laboratory studies how cells and antigens come together to generate immune responses. This involves a focus on deciphering the cues that guide immune cell movements within, and egress from, lymphoid organs. G-protein coupled receptors (GPCRs) are a major class of chemoattractant receptor on immune cells and we have used gain- and loss-of function approaches to establish roles for several GPCRs that respond to protein (chemokine), lipid (sphingosine-1-phosphate (S1P), oxysterol) and metabolite (S-geranylgeranyl-L-glutathione) ligands and to study how these responses adapt after exposure to antigen or inflammatory inputs. We established that lymphocyte egress from lymphoid organs is mediated by S1PR1 and defined mechanisms acting to maintain high S1P at egress sites. We have a strong interest in understanding how cell interaction dynamics influence the selection events underlying antibody affinity maturation. We use real-time intravital 2-photon microscopy to study these dynamics and are working on tools for the in vivo quantitation of cell-cell interaction and cell signaling in germinal centers. Our studies are also informative about pathways leading to lymphomagenesis. We study requirements for mounting long-lived antibody (plasma cell and memory B cell) responses and the derangements associated with autoantibody responses. We also explore requirements for barrier immunity at epithelial surfaces.