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, Co-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 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, then at the Mayo Clinic, 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 several types of tumors and that its activity can cause the death of T cells, thus preventing them from eliminating cancer cells. Bringing these lines of inquiry full circle, he later showed that blocking this interaction 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, when he moved to the Johns Hopkins Medical Institute, and developed PD-L1 staining as a biomarker to predict treatment outcome.  His discoveries directly led to the development of anti-PD-1/PD-L1 antibody therapy against broad spectrum of human cancers. These discoveries have 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 University 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. 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 Institute 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. Foxman's research interest is understanding the natural mechanisms that protect the airway from respiratory viruses. Recent evidence shows that respiratory viruses enter the airway much more frequently than they cause illness. Current projects focus on (1) identifying the antiviral defense mechanisms of the airway epithelium, (2) understanding how the environment influences antiviral defense and tips the balance between health and disease upon exposure to a virus, and (3) using biomarkers of the body's response to infection to diagnose the cause of respiratory symptoms.

Background. Dr. Foxman received her M.D. and Ph.D. training at Stanford University, and her residency training in Clinical Pathology, a medical specialty devoted to diagnostic testing, at Brigham and Women's Hospital in Boston, MA. Her postdoctoral studies in host-virus interactions were conducted with the mentorship of Akiko Iwasaki in the Department of Immunobiology at Yale. These studies demonstrated mechanisms whereby cool ambient temperature permits growth of the common cold virus by diminishing antiviral responses of airway epithelial cells. Dr. Foxman is currently an Assistant Professor in the Yale Department of Laboratory Medicine.

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 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. He has received numerous honors including the Dystel Prize from the AAN for his MS research and is among the most highly cited living neurologists.

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 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.

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.

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, founded in 1921 as the first Genetics Department in the country. At Wisconsin with Dr. Robert DeMars on 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).

At Yale she continued her studies on CD8 and recently has focused on the functional relevance of four isoforms of the 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. Signal transduction by the isoforms is different given that they differ only in their cytoplasmic tail. The clinical relevance of these isoforms for adoptive immunotherapy with T cells is one focus of the lab.

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 an Associate 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 signature of human infection and vaccination responses

Dr. Kriegel is an Assistant Professor of Immunobiology and of Medicine (Rheumatology) at Yale School of Medicine. In 2001, he received his MD/PhD equivalent at the Friedrich-Alexander University of Erlangen, Germany, followed by the German Medical Licensure in 2002. From 2003 to 2006, he performed postdoctoral training in immunology at Yale with Dr. Richard Flavell before completing a medicine residency and rheumatology fellowship at Harvard (Beth Israel Deaconess Medical Center and Brigham & Women’s Hospital). During this time, he performed additional postdoctoral research at Harvard Medical School with Drs. Diane Mathis and Christophe Benoist. Dr. Kriegel returned to Yale in 2012 as a tenure-track faculty member in the Department of Immunobiology. He is also a board-certified rheumatologist at Yale-New Haven Hospital and maintains a specialty clinic for antiphospholipid syndrome. His NIH-funded laboratory explores host-microbiota interactions in immune diseases by combining human microbiome studies with mechanistic work, which includes utilization of gnotobiotic models. He was an Emmy-Noether Scholar of the German Research Foundation, an Arthritis National Research Foundation Scholar, an awardee of the Lupus Research Institute, and the Arthritis Foundation. He serves as an Advisory Editor for Arthritis & Rheumatology and is a member of the American Association for the Advancement of Science, the German and American Association of Immunologists, the American College of Rheumatology, and the Society for Mucosal Immunology.

Dr. Carrie L. Lucas received her PhD from Harvard Medical School and her postdoctoral training from the National Institutes of Health, NIAID. Her laboratory investigates signaling in T cells from healthy people and patients with inherited immune disorders to dissect pathways critical for adaptive immunity. A major focus of her work has been on phosphoinositide 3-kinase (PI3K) signaling and mechanisms of disease in immunodeficient patients with activating mutations in PI3K subunits.

John MacMicking is a Howard Hughes Medical Institute (HHMI) Investigator. He trained in synthetic organic chemistry at the Australian National University (B.Sc, 1st Class Honors) where he conducted thesis work in the Department of Immunology & Cell Biology formerly headed by 1996 Nobel Laureate, Peter Doherty, at the the John Curtin School of Medical Research.

He then came to the U.S. to pursue Ph.D studies with Carl Nathan in the Immunology program at Cornell University-Sloan-Kettering Institute in New York City before being selected as an HHMI Life Science Research Foundation Fellow at The Rockefeller University to conduct studies with John Mckinney.

His doctoral dissertation described the first knockout of an innate immune gene in mammals - inducible nitric oxide synthase (iNOS) - genetically engineered between 1992-1995. It served as an early paradigm for cell-autonomous immunity to infection. At Rockefeller University he computationally identified, physically mapped and began functionally characterizing a complete IFN-inducible GTPase superfamily in humans and mice as a new defense network operating against all pathogen classes. For these discoveries he has been named a Edward Mallinckrodt Jr Foundation Fellow (2004), Searle Scholar (2005), Cancer Research Institute Investigator (2006), Burroughs-Wellcome Fund Investigator (2008), CCFA Senior Research Awardee (2010), AAF Scholar (2014) and Kenneth Rainin Foundation Innovator (2014).

Dr. MacMicking was promoted to Associate Professor in 2010 and received Tenure in 2014. He was chosen as an HHMI Investigator in 2015 before moving to the Yale Systems Biology Institute in 2017. 

Medzhitov was born in Tashkent, Uzbekistan, and earned a B.S. at Tashkent State University before going on to pursue a Ph.D. in biochemistry at Moscow University in 1990. He performed his postdoctoral studies with the late Charles A. Janeway Jr. at Yale University Medical School.

My work focuses on the etiology of autoimmune diseases affecting millions of individuals in the world by identifying molecules and pathways involved in the establishment of B-cell tolerance through the investigation of rare patients with primary immunodeficiency (PID), enrolled at Yale and through an international network.

Patients with PID provide opportunities to study the impact of specific gene defects on the regulation of B-cell tolerance and the removal of developing autoreactive B cells in humans. Using a RT-PCR based strategy that allows us to assess the frequency of autoreactive B cells, we found that alterations in B-cell receptor (BCR) signaling in patients lacking functional BTK or CD19, or mutations in molecules mediating TLR signaling such as TACI, IRAK4, MyD88 as well as in adenosine deaminase (ADA) and activation-induced cytidine deaminase (AID) all result in a defective central checkpoint and a failure to counterselect developing autoreactive B cells in the bone marrow. Interestingly, successful gene therapy in ADA-deficient patients results in the restoration of early B-cell tolerance checkpoints, revealing that appropriate regiments could correct B-cell selection impairments characteristic of many patients with autoimmune conditions. Our investigations also revealed that central B-cell tolerance defects are primary to many autoimmune diseases including rheumatoid arthritis, type 1 diabetes and systemic lupus erythematosus and can result from genetic polymorphisms such as the R620W PTPN22 risk allele associated with all these diseases and that was reported to alter BCR signaling important for the regulation of this checkpoint.

In contrast, most patients with multiple sclerosis only suffer from specific defects of their peripheral B-cell tolerance checkpoint that likely result from abnormal regulatory T cells, which normally control this second B-cell selection step in the periphery. Regardless of which early B-cell tolerance checkpoint is defective in patients with autoimmune diseases, all these patients are characterized by the accumulation of autoreactive clones in their mature naïve B cell compartment, which may contribute to the development of autoimmunity by increasing the frequency of B cells presenting self-antigens. Understanding the etiology of autoimmunity is the first step toward effective treatment, therapy and ultimately, cure.

Dr. Kevin C. O’Connor is an Associate Professor of Neurology and Immunobiology at Yale School of Medicine. He earned a Bachelor of Science degree in Chemistry from the University of Massachusetts at Amherst and his Ph.D. in Biochemistry at Tufts Medical School. He took his post-doctoral training in Immunology at Harvard Medical School where he also spent several years on the faculty as an Assistant Professor. His investigative interests are in human translational immunology and neurology. He and his group are specifically interested in defining the mechanisms by which B cells, and the antibodies they produce, affect tissue damage in autoimmunity. To this end they are engaged in understanding how particular B cell subsets initiate and sustain autoimmunity. He and his team were among the first to characterize tertiary lymphoid tissue and the adaptive immune response in germ cell tumors and meningiomas. They also described the molecular characteristics of B cells and plasma cells that populate the muscle tissue of patients with myositis. They refined the role of Epstein-Barr virus in the multiple sclerosis (MS) brain and have further defined the role of humoral immunity in children with MS. Recently, he and his team identified a network of B cells and autoantibodies that populate the MS central nervous system. His current research focus includes further defining the immunopathology of myasthenia gravis (MG). He and his team demonstrated that B cell depletion therapy has sustained efficacy in MG. They were the first to show that MG-derived AChR antigen specific T cells belong to the pro-inflammatory Th17 subset. They also determined that MG subjects harbor defects in B cell tolerance checkpoints that correlate with abnormalities in the naïve B cells repertoire. They most recently identified the autoantibody-producing cells in MuSK MG. Their current focus is on further defining the mechanisms of autoantibody production in MG with the aim of improving therapeutic approaches.

Noah W. Palm is an Assistant Professor of Immunobiology and a member of the Human and Translational Immunology Program at the Yale University School of Medicine. His laboratory focuses on illuminating the myriad interactions between the immune system and the gut microbiota in health and disease. Dr. Palm performed his doctoral work with Ruslan Medzhitov and his postdoctoral work with Richard Flavell, both at Yale University.

Dr. João P. Pereira is an associate professor of Immunobiology, member of the Yale Cancer Center and of the Yale Stem Cell Center.  He studied Microbiology at Universidade Católica Portuguesa (BSc, 1996), Biotechnology at DeMontfort University (MSc, 1997), and did PhD studies (Universidade do Porto, 2004) in Immunology at the Gulbenkian Institute (Oeiras) and the Pasteur Institute (Paris) mentored by Paulo Vieira. In 2005 Dr. Pereira joined the laboratory of Dr. Jason Cyster (UCSF) as a Howard Hughes Medical Institute Postdoctoral fellow.  In the Cyster lab he studied mechanisms of B lymphocyte migration during development in primary lymphoid organs and during activation in secondary lymphoid organs. Dr. Pereira joined the department of Immunobiology at Yale University in 2010.

Dr. Pober was born in Brooklyn, New York in 1949 and grew up in the New York City metropolitan area. He attended Haverford College, graduating summa cum laude in 1971 with high honors in Biology, Chemistry and History. He was admitted to Yale’s Medical Scientist Training Program, receiving his MD and his PhD in Molecular Biophysics and Biochemistry with Prof. Lubert Stryer in 1977. He completed his first year of pathology residency at Yale-New Haven Hospital in 1978, was a post-doctoral fellow with Prof. Jack Strominger in the Department of Biochemistry at Harvard University from 1978 through 1980, and completed pathology training at Brigham and Women’s Hospital in 1981. He worked as an attending Pathologist at Brigham and Women’s Hospital from 1981-1991, serving as an Assistant Professor and then Associate Professor of Pathology at Harvard Medical School during the same period.

He returned to Yale Medical School in 1991 as a Professor of Pathology and Immunobiology, and also became a Professor of Dermatology in 1998. Dr. Pober was named the Director of the Molecular Cardiobiology Program at the Boyer Center for Molecular Medicine in 1991 and founded the Vascular Biology and Transplantation (VBT) Program, which succeeded Molecular Cardiobiology, in 1999. In 2007, he stepped down as the director of the VBT program, becoming Professor and Vice-Chair of the Department of Immunobiology for the Section of Human and Translational Immunology. He was named Ensign Professor of Immunobiology in 2011 and Bayer Professor of Translational Medicine in 2012. Dr. Pober has been honored as a Searle Scholar, an Established Investigator of the American Heart Association and a MERIT awardee of the National Heart, Lung and Blood Institute. He received the Warner Lambert-Parke Davis award in 1988 and the Rous Whipple Award in 2011 from the American Society of Investigative Pathology, the Earl Benditt award from the North American Vascular Biology Organization in 2014 and the Basic Science Established Investigator Award from the American Society of Transplantation in 2018. He has served as an Editor of Immunity and Co-Editor-in Chief of Laboratory Investigation, leading immunology and pathology journals, respectively. He also has served as President of the North American Vascular Biology Organization. He is co-founder and co-director of the Joint Yale-Cambridge University Biomedical Research Program, is a visiting fellow in the Dept. of Medicine at the University of Cambridge, and was elected a Fellow Commoner of Trinity Hall, University of Cambridge in 2012. .

Dr. Pober’s research involves understanding the functions of blood vessels and vascular cells in human inflammatory and immune responses and, reciprocally, how inflammation and immunity affect vascular health and function. He is particularly interested in how insights from experiments with human cells and tissues and with humanized mice can be used to improve organ replacement therapy, to improve tissue engineering and to regenerate injured tissues.

Aaron Ring received his undergraduate training at Yale University and entered the Stanford Medical Scientist Training Program for his MD and PhD degrees. At Stanford, he worked in the laboratories of K. Christopher Garcia and Irving Weissman to use structure-based protein engineering to develop new cytokine and immune checkpoint therapies for cancer. He additionally developed novel methodologies in protein engineering to create biologic agents against challenging targets such as G protein coupled receptors (GPCRs). Aaron joined the faculty of the Yale Department of Immunobiology in 2016 as the Robert T. McCluskey Yale Scholar. The focus of his research is to understand and manipulate the activity of immune receptors using structural and combinatorial biology approaches.

Craig Roy received his B.S. from Michigan State University in 1985 and earned his Ph.D. in Microbiology and Immunology at Stanford University in 1991 in the laboratory of Dr. Stanley Falkow. After completing a postdoctoral fellowship with Dr. Ralph Isberg in the Department of Molecular Microbiology at Tufts University School of Medicine in 1996, he was appointed as an Assistant Professor in the Department of Molecular Genetics and Microbiology at Stony Brook University. Dr. Roy became a founding member of the Department of Microbial Pathogenesis at Yale University in 1998 and serves as Vice-Chair. He currently holds the title of Waldemar Von Zedtwitz Professor of Microbial Pathogenesis and Immunobiology. Research in the Roy laboratory focuses on the host-pathogen interface. Using multi-disciplinary approaches his laboratory has discovered many novel mechanisms that intracellular pathogens use to modulate host membrane transport pathways, which allow these pathogens to evade cell autonomous defenses and create novel organelles that permit bacterial replication.

Dr. Schatz has made fundamental contributions to our understanding of the mechanisms that assemble and diversify antigen receptor genes that encode antibodies and T cell receptors.  He is best known for the discovery of RAG1 and RAG2, subsequent biochemical insights into RAG function and evolutionary origins, and the discovery of two distinct levels of regulation of somatic hypermutation.

Schatz has co-authored over 160 articles, many in prestigious journals, and has been the recipient of numerous prizes and awards, including the Rhodes Scholarship, the Snow Prize (Yale University's top award to a graduating senior), the National Science Foundation Presidential Faculty Fellows Award, the American Association of Immunologists-BD Biosciences Investigator Award, and election to the National Academy of Sciences. He has been active as an editor and reviewer, serving as Co-Editor of the journal Immunity, as a member of the editorial board of a number of journals, and as a member and Chair of the NIH study section Cellular and Molecular Immunology-A.  Schatz has also been very interested in graduate education, serving for many years as the Director of Graduate Studies and Graduate Admissions for Immunobiology and as a member of the Executive Committee of the Biological and Biomedical Sciences (BBS) Program.  He remains strongly committed to enhancing predoctoral and postdoctoral training programs in his current role as Chair of the Department of Immunobiology.

Schatz received B.S. and M.S. degrees in Molecular Biophysics and Biochemistry from Yale University in 1980, and a M.A. degree in Philosophy and Politics from Oxford University in 1982. His Ph.D. degree (1990) and postdoctoral training were done with Dr. David Baltimore at the Massachusetts Institute of Technology and the Whitehead Institute for Biomedical Research.

Dr. Wilen received his A.B in Biology and Economics at Washington University in St. Louis, his MD and PhD from the University of Pennsylvania. His residency training was in clinical pathology at Barnes-Jewish Hospital in St. Louis, MO. His postdoctoral studies were conducted in the laboratory of Herbert "Skip" Virgin in the Department of Pathology & Immunology at Washington University School of Medicine where he studied the pathogenesis of norovirus, the leading cause of acute gastroenteritis globally. Specifically, he discovered CD300lf as the first receptor for a norovirus and identified intestinal tuft cells as the physiologic target cell for mouse norovirus infection. Dr. Wilen is currently an Assistant Professor in Laboratory Medicine and Immunobiology.

https://wilenlab.com