Richard Locksley is an immunologist recognized for his work in cytokine biology, with a particular interest in allergic immunity. His contributions include elucidation of networks of cells and cytokines that underpin allergic inflammation and the discoveries of unsuspected cellular constituents of allergy that play roles in tissue homeostasis. Locksley was born in Minneapolis, MN, in a military family, and grew up amid frequent travel. He attended Kent School in CT and graduated from Harvard College in 1970. After graduating from the University of Rochester School of Medicine, he was a resident and Chief Resident in Internal Medicine at UCSF in San Francisco. He pursued Infectious Diseases fellowship training at the University of Washington in Seattle, where he joined the faculty as an Assistant Professor in 1983. He was recruited back to UCSF to be Chief of Infectious Diseases in 1986, and was appointed Director of the Sandler Asthma Basic Research Center at UCSF in 2004. Locksley has been an Investigator of the Howard Hughes Medical Institute since 1997. He is a member of the American Society for Clinical Investigation, the Association of American Physicians, and the American Academy of Arts and Sciences, and is a Fellow in the American Academy of Microbiology.

Research Interests

Richard Locksley's laboratory is interested in pathways underlying the elicitation of allergic immunity. His laboratory contributed to the understanding of subsets of helper T cells that lead to different types of immune responses, and to the discovery in 2010 of Group 2 innate lymphoid cells, or ILC2s, whose biology remains a major focus of investigation. Using novel strains of mice genetically manipulated to reveal cellular production of short-lived cytokines, the Locksley lab has been able to establish pathways mediated by ILC2s that contribute to basal physiology and tissue health. These studies have revealed unexpected roles for these rare innate lymphoid cells in adipose tissue and systemic metabolic homeostasis, and in epithelia of the lung, small intestine, and other organs where cytokines from ILC2s activate gene programs in epithelial cells important in controlling the physical barrier separating tissues from the outside world. In the lung, ILC2s enhance secretion by specialized lung epithelial cells of chitinase, which degrades ubiquitous, environmentally acquired, insoluble chitin polysaccharides that induce lung inflammation. In the small intestine, ILC2s relay signals from tuft cells, rare epithelial cells that transduce luminal signals from the gut through ILC2s, which regulate cell-fate decisions of intestinal crypt progenitor cells.

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Primary Section

Section 43: Immunology and Inflammation