Our People

Marcus Bosenberg M.D., Ph.D., is a physician scientist who directs a leading melanoma research laboratory, is Co-Leader of the Genomics, Genetics and Epigenetics Program of the Yale Cancer Center, Director of the Yale SPORE in Skin Cancer, and is a practicing dermatopathologist at Yale Dermatopathology through Yale Medicine.

In his research, Dr. Bosenberg studies the genetics and cellular changes that result in melanoma, the leading cause of skin cancer deaths. His laboratory has developed several widely utilized mouse models in order to study how melanoma forms and progresses, to test new melanoma therapies, and how the immune system can be stimulated to fight melanoma. He works to translate basic scientific findings into improvements in melanoma diagnosis and therapy. He has published over 100 peer-reviewed articles, is a member of the Yale Cancer Center Executive Committee, and is a faculty member of the Raymond and Beverly Sackler Institute for Biological, Physical, and Engineering Sciences.

Dr. Bosenberg mentors undergraduate, graduate, medical, and MD-PhD students in his laboratory, teaches at Yale School of Medicine, and trains resident physicians, fellows, and postdoctoral fellows.

Al Bothwell graduated with an A.B. from Washington University in 1971, got a PhD from Yale in Sidney Altman’s lab in 1975 and then did a postdoc with David Baltimore at MIT where he established the genetic basis of the anti-NP idiotypic antibody response. He has been on the Immunobiology faculty at the Yale Medical School since 1982. He continued studies of B cell antibody diversity and memory and then worked on T cell receptor structure/function and signaling. He also developed the molecular genetics of the Ly6 gene family (aka Sca-1/Ly6A and Ly6C). Increasingly his work has shifted to studies of human immunity with development of humanized mouse models of vascular disease/transplantation, type 1 diabetes and cancer. Studies on gut inflammation in a genetic tumor model and Inflammatory Bowel Disease have lead most recently to contributions concerning wnt signaling to infections and asthma. His studies focus on the remarkable immunoregulatory properties of Wnt signaling that is both canonical and non-canonical and involves direct interaction with platelets.This is a basic mechanism for regulating tissue permeability affecting the mobility of lymphocytes and tumor cells.

Grace Chen received her undergraduate training in the College of Chemistry at UC Berkeley. She attended Harvard University for her PhD where she worked in David Liu's laboratory to discover and characterize novel RNA modifications. Her postdoctoral research was at Stanford University in Howard Chang's group, where she investigated circular RNA immunity. Grace Chen joined Yale University as a faculty in the Department of Immunobiology in 2019. Her research focuses on the functions and regulations of circular RNAs and RNA modifications in health and disease.

Lieping Chen studies immune cell communications via cell surface protein-protein interactions. He is also interested in translating laboratory findings to treat human diseases including cancer, autoimmune diseases and infection. 

In 1992, Dr. Chen showed the first proof-of-concept study that the B7-CD28 family molecules could be the targets for cancer immunotherapy. This study inspires subsequent studies targeting the B7-CD28 family molecules for the treatment of human cancer.

In 1999, Dr. Chen first to discover a molecule he called B7-H1, which is now also known as PD-L1. He subsequently showed that PD-L1 is expressed by tumors and that its activity can cause T cell dysfunction, thus preventing T cells from eliminating cancer cells. Bringing these lines of inquiry full circle, he later showed that blocking theinteraction between PD-1 and PD-L1 by monoclonal antibodies improved the immune system’s ability to eliminate tumors in a 2002 paper. Chen’s work provided an important foundation for the subsequent development of immunotherapies designed to block this activity, and thereby enable more effective immune responses against cancer. Dr. Chen also initiated and help organized the first-in-man clinical trial of anti-PD-1 monoclonal antibody for treating human cancer in 2006 and developed PD-L1 staining as a biomarker.  His discoveries directly led to the development of anti-PD-1/PD-L1 antibody therapy against broad spectrum of human cancers, which has revolutionized cancer treatment.

Other important breakthroughs made by Dr. Chen's laboratory include the development of an agonist antibody against the 4-1BB co-stimulatory pathway, also known as CD137. Multiple 4-1BB-targeting antibodies have since been developed and are now being evaluated in clinical trials for a variety of cancer types. Dr. Chen’s laboratory also discovered various molecular pathways with T cell costimulatory and coinhibitory functions and/or their applications in human disease treatment. These pathways include B7-H2 (ICOSL), B7-H3, B7-H4, B7-H5/CD28H, PD-1H (VISTA), TNFRSF19, RELT, LIGHT/HVEM, B7-H2/CD28/CTLA-4 (human), SALM5/HVEM, FGL1/LAG-3, Siglec-15 etc. Many of these findings are now being developed clinically for the treatment of human diseases.

Dr. Joseph Craft is Paul B. Beeson Professor of Medicine and Professor of Immunobiology at the Yale School of Medicine, and past chief of the Section of Rheumatology at Yale. He received his degrees in chemistry as a Phi Beta Kappa graduate of University of North Carolina at Chapel Hill and in medicine as an Alpha Omega Alpha graduate of the University of North Carolina School of Medicine. Dr. Craft did postgraduate training in internal medicine and in rheumatology and immunology at Yale, and has been on the faculty at that institution since 1985. At Yale, he teaches undergraduate, graduate, and medical students. He directs a research laboratory devoted to understanding the immune response to pathogens and vaccines, and dissecting and treating autoimmune diseases, such as systemic lupus erythematosus, with a primary focus upon the differentiation, metabolism, and function and regulation of T cells that promote B cell maturation in secondary lymphoid organs. His research has been continually supported by the National Institutes of Health since 1985, and he is a two-time R37 (MERIT) Awardee. He has been a primary mentor for over 20 postdoctoral fellows and for 21 PhD and MD/PhD graduate students, including 7 graduate students currently in his lab. Dr. Craft is Director of the Investigative Medicine Program at Yale, a unique program designed to provide Ph.D. training for physicians, and in his capacity as Director of the program and its Director of Graduate Studies, has supervised training of over 50 Investigative Medicine PhD students. Dr. Craft is recipient of the Bohmfalk Teaching Prize at Yale School of Medicine for outstanding teaching in the basic sciences. He is an elected Fellow of the American Association for the Advancement of Science, and an elected member of the American Society for Clinical Investigation and the Kunkel Society. Dr. Craft also is a member of the Board of Lupus Therapeutics of the Lupus Research Alliance, devoted to initiating novel therapeutic trials in lupus, and past Chair of the Board of Scientific Counselors at the National Institute of Arthritis, Musculoskeletal, and Skin Diseases (NIAMS). He is former chair of the Immunological Sciences (now HAI) and current member of the Arthritis, Connective Tissue and Skin Diseases (ACTS) standing study sections at NIH, past chair of the Scientific Advisory Board of the Alliance for Lupus Research, and a former Pew Scholar in the Biomedical Sciences and Kirkland Scholar. He is co-founder of L²Diagnostics, a company in New Haven, CT, formed in partnership with Yale University and devoted to discovery of new diagnostics and therapeutic targets for immunological and infectious diseases, and is currently a member of its Board of Directors.

Dr. Cresswell is the Eugene Higgins Professor of Immunobiology and Professor of Cell Biology and Dermatology at Yale University School of Medicine.

He received his B.S. degree in chemistry, his M.S. degree in microbiology from the University of Newcastle Upon Tyne, U.K., and his Ph.D. degree in biochemistry and immunology from London University. His postdoctoral training was completed at Harvard University with Jack Strominger.

Before assuming his position at Yale, Dr. Cresswell was Chief of the Division of Immunology at Duke University Medical Center. He is a Fellow of the Royal Society, U.K., and a member of the National Academy of Sciences, the American Academy of Arts and Sciences, and the Institute of Medicine.

Vishwa Deep Dixit completed Bachelor and Master of Veterinary Sciences in HAU, Hisar India. He received German Academic Exchange Service fellowship to conduct PhD research in Germany. He completed PhD coursework in HAU and Research Work in University of Hannover in Year 2000. He conducted postdoctoral research training in NIH. He joined Pennington Biomedical Research Center as an Assistant Professor in 2006 and moved to Yale as Professor of Comparative Medicine and Immunobiology in 2013. Dixit’s research is focused on understanding the interactions between metabolic and immune systems with the goal to reveal molecular targets that can be harnessed to control inflammation and immune dysfunction as means to enhance the healthspan. The research in Dixit Laboratory is funded by the National Institutes of Health, Glenn Foundation for Aging Research and Cure for Alzheimer Foundation.

Dr. Eisenbarth’s laboratory focuses on how dendritic cells, B cells and T cells interact to induce tailored adaptive immune responses. The work spans how this triad is operational in the spleen to transfused red blood cells (RBCs), in the lung to aeroallergens, and in the gut to food allergens, utilizing both mouse models and human samples.

https://eisenbarthlab.com/

Dr. Flavell is Sterling Professor of Immunobiology at Yale University School of Medicine, and an Investigator of the Howard Hughes Medical Institute. He received his B.Sc. (Honors) in 1967 and Ph.D. in 1970 in biochemistry from the University of Hull, England, and performed postdoctoral work in Amsterdam (1970-72) with Piet Borst and in Zurich (1972-73) with Charles Weissmann. Before accepting his current position in 1988, Dr. Flavell was first Assistant Professor (equivalent) at the University of Amsterdam (1974-79); then Head of the Laboratory of Gene Structure and Expression at the National Institute for Medical Research, Mill Hill, London (1979-82); and subsequently President and Chief Scientific Officer of Biogen Research Corporation, Cambridge, Massachusetts (1982-88). Dr. Flavell is a fellow of the Royal Society, a member of the National Academy of Sciences as well as the National Academy of Medicine. Richard Flavell uses transgenic and gene-targeted mice to study Innate and Adaptive immunity, T cell tolerance and activation in immunity and autoimmunity,apoptosis, and regulation of T cell differentiation.

Dr. Ellen Foxman, M.D., PhD. is an Assistant Professor of Laboratory Medicine and Immunobiology at the Yale School of Medicine. Her laboratory studies the fundamental biology of the airway epithelial development and innate immune signaling, and implications for the diagnosis and prevention of viral respiratory illness. 

Background. Dr. Foxman is an immunologist and clinical pathologist. She trained in medicine and immunology at Stanford University.  In Dr. Eugene Butcher’s group, she investigated leukocyte homing and the role of short term memory of prior chemotactic signals in allowing neutrophils to reach their target sites within tissues.   She became interested in respiratory viruses during her residency training in clinical pathology at Harvard's Brigham and Women's Hospital, due to the advances in testing that were beginning to reveal a previously unappreciated very high prevalence of these viruses.  She later joined Dr. Akiko Iwasaki’s group at Yale as a post-doctoral associate, where she studied antiviral innate immunity, demonstrating suppression of innate immune responses in the airway epithelium by cool ambient temperature.  In 2016, she established her independent research group studying host-virus interactions in the respiratory tract.

Ph.D., University of Pennsylvania (1992)

Dr. Hafler is the William S. and Lois Stiles Edgerly Professor and Chairman Department of Neurology, Yale School of Medicine and is the Neurologist-in-Chief of the Yale-New Haven Hospital. He graduated magna cum laude in 1974 from Emory University with combined B.S. and M.Sc. degrees in biochemistry, and the University of Miami School of Medicine in 1978. He then completed his internship in internal medicine at Johns Hopkins followed by a neurology residency at Cornell Medical Center-New York Hospital in New York.

Dr. Hafler received training in immunology at the Rockefeller University then at Harvard where he joined the faculty in 1984. He was one of the Executive Directors of the Program in Immunology at Harvard Medical School and was on the faculty of the Harvard-MIT Health Science and Technology program where he was actively involved in the training of graduate students and post-doctoral fellows.

Hafler, in many respects, is credited with identifying the central mechanisms underlying the likely cause of MS. His early seminal work demonstrated that the disease began in the blood, not the brain, which eventually led to the development of Tysabri to treat the disease by blocking the movement of immune cells from the blood to the brain. He was the first to identify myelin-reactive T cells in the disease, published in Nature, showing that indeed, MS was an autoimmune disorder. He then went on to show why autoreactive T cells were dysregulated by the first identification of regulatory T cells in humans followed by demonstration of their dysfunctional state in MS. As a founding, Broad Institute associate member, Hafler identified the genes that cause MS, published in the New England Journal of Medicine and Nature. More recently, he identified the key transcription factors and signaling pathways associated with MS genes as potential treatment targets. Finally, he recently discovered that salt drives induction of these pathogenic myelin reactive T cells, both works published in Nature. Hafler was the Breakstone Professor of Neuroscience at Harvard, and became Chairman of Neurology at Yale in 2009, where he has built an outstanding clinical and research program that strongly integrates medical sciences. Hafler is among the most highly cited living neurologists and has received numerous honors including the Dystel Prize from the AAN for his MS research, the Raymond Adams Award from the ANA, and was the recipient of the NIH Javits Investigator Award, and The Dale McFarlin Prize by the International Society of Neuroimmunology. He is a member of AOA, the American Society of Clinical Investigation, and was elected into the National Academy of Medicine.

My background and research are in translational immunology. I am interested in understanding the basis for autoimmune diseases and developing new therapies based on our understanding of disease mechanisms. My focus has largely been in the field of autoimmune Type 1 diabetes. The work encompasses basic laboratory work as well as clinical studies to understanding the regulation of autoreactive T cells to clinical trials that involve novel therapeutics. As part of these studies I have also been very interested in analysis of beta cell function in Type 1 diabetes. As part of this interest, we have been studying the development of autoimmune diabetes in patients with cancers who are treated with checkpoint inhibitors. Our clinical and basic studies are focused on understanding how beta cells are destroyed and react to inflammation. Finally, with the COVID-19 pandemic, we have been studying the immunologic basis for responses in children and adults who are hospitalized with COVID-19 to understand the mechanisms that can lead to disease protection. 

Akiko Iwasaki received her Ph.D. from the University of Toronto (Canada) in 1998, and her postdoctoral training from the National Institutes of Health (USA) (1998-2000). She joined Yale University (USA) as a faculty in 2000, and currently is an Investigator of the HHMI and Waldemar Von Zedtwitz Professor of Department of Immunobiology, and of Department of Molecular Cellular and Developmental Biology. Akiko Iwasaki’s research focuses on the mechanisms of immune defense against viruses at the mucosal surfaces. Her laboratory is interested in how innate recognition of viral infections lead to the generation of adaptive immunity, and how adaptive immunity mediates protection against subsequent viral challenge.

I am a physician-scientist in the Section of Cardiovascular Medicine. My research laboratory studies the role of endothelial cells, the cells that line blood vessels, in solid organ transplant rejection. In this endeavor, we have developed novel, patient-centered protocols heavily incorporating human biospecimens to increase the likelihood that findings derived from these assays will be clinically relevant.

My laboratory uses intricate tumor models and advanced approaches to investigate immune cell interactions with developing tumors. My goal is to determine mechanistically why these interactions do not lead to more potent anti-tumor responses and to identify entry points for modulating these interactions through genetic manipulation and therapeutic intervention. My previous studies have focused on using established complex mouse models to investigate how subtypes of T cells in the tumor microenvironment impact tumor development. My laboratory will combine advanced genetic modeling of mice and immunologic techniques to address fundamental questions in tumor immunology.

Dr. Kavathas graduated with a B.A. in American Institutions, from the University of Wisconsin, writing her thesis on the role of Science in America in the 1960s. She obtained her Ph.D. in Genetics from the Department of Genetics, with Dr. Robert DeMars performing a genetic analysis of the MHC region. As a postdoctoral fellowship at Stanford University with Dr. Leonard Herzenberg she developed a novel approach for cloning genes for cell surface proteins using the fluorescence activated cell sorter (FACS) and cloned the gene for the human CD8 protein.

At Yale she continued her studies on CD8ab, a cell surface protein that functions as a co-receptor with the T Cell receptor on CD8 killer T cells.  Her lab characterized the expression and functional differences of  four isoforms of the human CD8b protein that exist in humans and great apes but not mice. They are differentially expressed in naive T cells, activated T cells, and memory T cells and they show differences in signal transduction and modification by ubiquitination.  More recently she is studying how to enhance killing of human lung cancer tumors that have lost expression of HLA class I and are no longer killed by CD8 T killer cells. 

Dr. Steven Kleinstein is a computational immunologist with a combination of "big data" analysis and immunology domain expertise. His research interests include both developing new computational methods and applying these methods to study human immune responses. Dr. Kleinstein received a B.A.S. in Computer Science from the University of Pennsylvania and a Ph.D. in Computer Science from Princeton University. He is currently Professor of Pathology (with a secondary appointment in Immunobiology) at the Yale School of Medicine, and a member of the Interdepartmental Program in Computational Biology and Bioinformatics (CBB), and the Human and Translational Immunology Program. 

Specific areas of research focus include:

• High-throughput B cell receptor (BCR) repertoire profiling (AIRR-seq or Rep-seq)
• Immune signatures of human infection and vaccination responses

Dr. Carrie L. Lucas received her PhD from Harvard Medical School and her postdoctoral training from the National Institutes of Health, NIAID. Her laboratory discovers single-gene defects underlying severe immune disorders in humans and investigates mechanisms using patient cells and genetically engineered mouse models. A major focus of her work has been on phosphoinositide 3-kinase (PI3K) signaling and mechanisms of disease in immunodeficient patients with mutations in PI3K subunits.