About the Cover
The ability of T cells to accumulate among cancer cells is impaired in many cancers. T-cell exclusion from the “cancer cell nests” may account for the failure of systemic immunity to control tumor growth, and for the absence of a response to checkpoint antagonist anti–PD-L1 in the murine model of pancreatic ductal adenocarcinoma (PDA). Recent studies have shown that fibroblast-like stromal cells, termed carcinoma-associated fibroblasts (CAF), in the tumor microenvironment exert an immune-suppressive function, and the depletion of CAF permits tumor infiltration of T cells and control of PDA tumors. PDA cancer cells are p53⁺ because they contain stable p53R172H proteins due to the loss of the wild-type p53 allele. The cover image is a confocal immunofluorescence photomicrograph of a mouse PDA containing epithelial cells (stained green for cytokeratin 19), p53⁺ cancer cells (silver), and CAF that express fibroblast-activating protein-α (FAP; red). All nuclei are stained blue with DAPI. For details, see the Masters of Immunology article by Douglas T. Fearon on page 187 of this issue.

About the Master
Douglas T. Fearon, MD, FRS, is the Emeritus Sheila Joan Smith Professor of Immunology at the University of Cambridge, UK, and senior group leader at the Cancer Research UK Cambridge Institute. He received his medical degree at the Johns Hopkins University School of Medicine, followed by internship and residency in internal medicine at the Johns Hopkins Hospital (Baltimore, MD). His scientific training began in 1972 when he joined Dr. Frank Austen's laboratory at Harvard Medical School (HMS) and the Robert bent Brigham Hospital (now part of the Brigham and Women’s Hospital) in Boston, MA, as a clinical research fellow in rheumatology and immunology. During this time, Dr. Fearon learned the fundamentals of basic research; he studied innate immunity, identifying and characterizing components of the complement system that enhance immune responses and support antibody functions. He became a full professor at HMS in 1984.
Dr. Fearon returned to Johns Hopkins School of Medicine in 1987, where he developed and directed the graduate program in immunology. During this period, the Fearon laboratory studied various aspects of adaptive immunity and B-cell and T-cell biology, culminating in the identification of complement C3d as a molecular adjuvant that bridges the innate and adaptive immunity. In 1993, ending his dual role as clinician and scientist, Dr. Fearon moved his laboratory to the University of Cambridge to work as a full-time researcher. The Fearon laboratory has been exploring the means by which tumors escape control by the immune system. Currently they focus on the role of the carcinoma-associated fibroblast that is identified by its expression of fibroblast activation protein in the tumor microenvironment and immune control of tumor growth.
Dr. Fearon received his BA cum laude with honors in English literature from Williams College (Williamstown, MA) while quarterbacking for the college's football team. After completing his medical training at Johns Hopkins in 1970, Dr. Fearon served as a major in the U.S. Army Medical Corps for two years, one of which was spent in Vietnam, and he received the Bronze Star for his efforts at helping soldiers overcome heroin addiction. He was elected a fellow of both the UK Royal Society and the Academy of Medical Sciences and a member of both the U.S. National Academy of Sciences and the American Academy of Arts and Sciences. Dr. Fearon has published over 140 peer-reviewed research papers and 78 reviews.