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In 1999, I became chair of the Department of Pathology (and finished my tenure in that role on April 30, 2016), the Mary Hewitt Loveless, MD Professor, and a professor of pathology and of microbiology and immunology at Stanford University School of Medicine. I am also a member of the Executive Committee of the Stanford Institute for Immunity, Transplantation and Infection. From 2009-2016, while chair of pathology, I also was Co-Director of the Stanford Center for Genomics and Personalized Medicine.I received a BA in biology in 1968 from Harvard College, a BMS in 1970 from Dartmouth Medical School (then a two year school) and the MD in 1973 from Harvard Medical School (HMS), and completed a residency and chief residency in Anatomic Pathology at Massachusetts General Hospital (MGH) in 1977. After postdoctoral training with Harold F. Dvorak at MGH, I joined the HMS faculty in 1979 as assistant professor of pathology, became professor of pathology in 1993, and, until moving to Stanford, served as director of the Division of Experimental Pathology at Beth Israel Deaconess Medical Center and a member of the HMS Committee on Immunology. My research focuses on the development and function of mast cells and basophils (major effector cells in allergic disorders) and the development of new animal models for studying the roles of these cells in health and disease. I have particular interests in the roles of these cells in anaphylaxis, food allergies, and asthma, and in the roles of mast cells and IgE in innate and acquired host defense against venoms.
Mast cells, which normally reside in the tissues, and basophils, which circulate in the blood, are major effector cells of asthma and other IgE-associated allergic disorders (e.g., anaphylaxis, food allergy, allergic rhinitis, atopic dermatitis, and asthma) and in immune responses to parasites. However, mast cells also have been implicated (as effector and/or immunoregulatory cells) in many other settings. For example, our lab has shown that mast cells can enhance innate and acquired immune responses that help to reduce the toxicity and mortality induced by arthropod and reptile venoms, which may represent a major evolutionary benefit of mast cells (and IgE antibodies). There also is evidence that mast cells can contribute to host responses to pathogens other than parasites, such as bacteria and viruses, and can have potential beneficial or harmful effects in diverse immnunological or inflammatory disorders that are not thought to involve IgE. Finally, mast cells have been implicated in many processes that maintain homeostasis or regulate tissue remodeling, such as angiogenesis, wound healing, the regulation of epithelial and mesenchymal cell development and function, and interactions with sensory nerves. The goals of Dr. Galli's laboratory are to develop and employ genetic approaches in mice to understand the regulation of mast cell and basophil development and the expression of mast cell and basophil function, and to elucidate the roles of these cells in health and disease. In parallel with these mouse studies, we investigate the roles of mast cells and basophils in human health and disease by conducting studies of human mast cells and basophils in vitro, or by analyzing specimens derived from patients with food allergy, asthma, atopic dermatitis, or other disorders in which mast cells or basophils have been implicated. In addition to studies focused on mast cells and basophils, the Galli lab also analyzes immunological mechanisms which underlie the development of severe allergies, such as those to certain foods, and the immunological regulatory mechanisms that can be engaged therapeutically to reduce the severity of these disorders or ameliorate them, e.g., via the induction of desensitization or tolerance. Finally, we are attempting to define "biomarkers", such as changes in the levels of surface structures on circulating basophils, which can be used to monitor the severity of allergic disorders and/or the patients' responses to immunotherapy or other therapeutic interventions.