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Dr Jyothi Rengaragan


Dr. Jyothi Rengarajan is an Associate Professor of Medicine at the Emory University School of Medicine and the Emory Vaccine Center. Her research program centers on understanding the mechanisms of Mycobacterium tuberculosis pathogenesis and host immunity to infection in animal models and humans. Using a combination of functional genomics, proteomics, microbiologic and immunologic approaches, her group studies M. tuberculosis mechanisms involved in evading host immunity and novel strategies for developing vaccines and therapeutics for TB. Dr. Rengarajan also conducts translational patient-based research through collaborative partnerships in the U.S, South Africa, India and Brazil to study human immunity to latent and active TB. Her research has identified human biomarkers of latent, active and clinically resolved TB that could improve TB diagnostics and accelerate monitoring response to anti-TB treatment. In addition, her group is interested in understanding how HIV co-infection perturbs latency to drive progression to TB disease in humans and how SIV perturbs innate and adaptive immunity in a rhesus macaque model of M. tuberculosis infection.​

Dr Delia Goletti MD, PhD


Head of the Translation Research Unit
National Institute for Infectious Disease L. Spallanzani, Rome, Italy

Dr Goletti works on tuberculosis (TB) research focusing on immune pathogenesis, TB immunodiagnostic tests, biomarkers, autophagy, and impact of Helminth infection on HIV and TB disease, impact of immune suppressive therapy on the infectious diseases development. She recently started working on the immune pathogenesis of Echinococcosis. She has ongoing collaborations with several groups worldwide (India, Africa, Europe) working on the translational aspects of TB immune assays. She collaborates with the World Health Organization (WHO) and European Respiratory Society (ERS) for the project on TB elimination in low incidence countries. She collaborates with the New Diagnostics Working Group Task Force on Tests for progression of LTBI to active disease supported by WHO and FIND. She has a European patent (N. 1723426) on an assay of immune diagnosis of tuberculosis and on the monitoring of therapy efficacy of tuberculosis. She is academic editor of Journal of Infection, BMC Infectious Diseases, PLoS ONE, Peer J, Translational Biomedicine, Autoimmune Diseases and Therapeutic Approaches. She is present in the list of the top Italian scientists from 2014.​​​​

​​​​​​​​Dr Dan Barber, PhD


Chief, T-Lymphocyte Biology Unit
Laboratory of Parasitic Diseases
National Institute of Allergy and Infectious Diseases
National Institutes of Health

The primary goal of the Barber laboratory is to understand the protective and pathogenic functions of Mtb-specific CD4 T cells. In particular, we have a major interest in the cell-surface inhibitory receptor PD-1. PD-1 is a co-inhibitory member of the CD28 family that plays a major role in attenuating CD4 and CD8 T-cell effector functions during chronic viral, bacterial, and fungal infections, as well as in cancer. Blockade of the PD-1 pathway has been shown to boost T-cell responses and enhance clearance of pathogens and tumors. However, inhibitory signals through PD-1 also play a major beneficial role in regulating autoreactive T-cells and sometimes are critical for preventing damaging immunopathology during infection. Our recent work has shown that, in the case of Mtb infection, the absence of PD-1 causes CD4 T-cell responses to switch from host-protective to detrimental and actually drive fatal disease. This illustrates how not only the generation but also the appropriate negative regulation of T-cell responses is critical during Mtb infection. A major goal is to characterize the mechanisms through which regulatory pathways, including PD-1, facilitate T-cell-dependent control or exacerbation of Mtb infection.

M. tuberculosis and M. avium are common causes of morbidity and mortality in HIV-infected patients due to the requirement for Th1 cells in control of mycobacterial infections, and antiretroviral therapy (ART) usually restores CD4 T-cell-dependent protective immunity. However, instead of the expected improvement in symptoms, HIV patients with co-infections sometimes experience a rapid deterioration, referred to as immune reconstitution inflammatory syndrome (IRIS), soon after initiating ART. IRIS has become a major problem in the clinical management of the HIV pandemic, and very little is understood about the mechanisms of pathology or factors determining the susceptibility to IRIS. We have developed a robust model of experimentally induced IRIS in M. avium-infected, T-cell-deficient mice. A major goal of the Barber laboratory will be to use this system to define the basic principles of IRIS, with the aim of generating hypotheses that can be tested in IRIS patients. Understanding CD4 T-cell repopulation of microbial-infected lymphopenic hosts may lead to novel therapeutic approaches that prevent IRIS and further decrease morbidity and mortality in HIV patients during ART.

​​​​​​​​Dr Andrea Cooper, PhD


Professor of Cellular Immunology
Department of Infection, Immunity and Inflammation
University of Leicester

Professor Cooper received her undergraduate degree from University College, London and her Doctoral degree from The London School of Hygiene and Tropical Medicine UK, where she investigated the interaction between macrophages and protozoan parasites of the genus Leishmania. Moving to the National Institutes of Health in Bethesda, Maryland, US she expanded her investigation of leishmaniasis to include the T cell response of patients suffering from cutaneous, mucocutaneous and visceral forms of this disease. She then moved to the Mycobacterial Research Labs at Colorado State University and began studying the protective immune response to Mycobacterium tuberculosis. Prior to her move to the University of Leicester she was at the Trudeau Institute, Inc. for 12 years where she held the E.L. Trudeau Chair which allowed her to study the cellular immune response to Mycobacterium tuberculosis. The goal of Professor Cooper’s programme at the University of Leicester is to define the factors impacting expression of immunity in the lung. The underlying themes include:

  • The role of early innate events in driving coordinated immune responses.
  • The role of cytokines and chemokines in initiation, expression and regulation of immunity.
  • The role of lymphocyte priming, differentiation and migratory capacity in prolonged expression of immunity.
  • The role of the inflamed environment in regulating the expression of immunity.

The infection model of choice is mycobacterial challenge through droplet particles to the alveolar tissue in the lung. This model uses a low dose challenge, allowing for very early immune-mediated events in the lung tissue to be dissected with regard to kinetics, location and the contribution of specific cell types to immunity. There has been a focus on the role of IL-12, IL-23 and IL-17 and the specific role of dendritic cells and lung resident innate lymphocytes in initiation and coordination of the acquired T cell response. A newer project involves examination of the role of neonatal exposure to bacterial products as a factor which impacts early responses to mycobacterial infection in the adult. These studies impact on working models of what makes individuals more susceptible to infection in the lung and also to our understanding of basic immune mechanisms. ​

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​​​​​​​​Dr Helen Fletcher BSc PhD


​Senior Lecturer in Immunology and Director, TB Centre
London School of Hygiene and Tropical Medicine, UK

Dr Fletcher gained a PhD in Medical Microbiology from the University of Leeds and became interested in tuberculosis (TB) in 1999 during her first postdoctoral position at University College London. In 2002 she moved to the Jenner Institute at the University of Oxford as an immunologist for the first-in-man trial of a new TB vaccine, MVA85A. After 10 ​years at the Jenner Institute she moved to the London School of Hygiene & Tropical Medicine to establish her group, based in the Immunology and Infection Department, which focuses on immune correlates and the host response to TB vaccination. In 2015 she became Director of the TB Centre: at the London School of Hygiene & Tropical Medicine and in 2016 became co-chair of the T-cell Immunology working group for the Collaboration for TB Vaccine Discovery (CTVD) at the Bill & Melinda Gates Foundation.​

Dr Robert L. Modlin, MD


Klein Professor of Dermatology
Professor of Microbiology, Immunology and Molecular Genetics
Chief of the Division of Dermatology
Vice Chair for Cutaneous Medicine and Dermatologic Research in the Department of Medicine
David Geffen School of Medicine, University of California, Los Angeles

Dr Modlin completed his undergraduate studies at Johns Hopkins University. He received his medical degree at the New York University (NYU) School of Medicine. Modlin was a pediatrics intern at NYU and a dermatology resident at Los Angeles County/University of Southern California School of Medicine. Dr. Modlin's primary research mentor is Barry R. Bloom, Ph.D. Since 1990, Dr. Modlin's interest in leprosy began during his dermatology residency at the Los Angeles County/University of Southern California Medical Center, learning from Dr. Thomas Rea. The goal of his research is using the study of leprosy as a model to learn about mechanisms of host defense in humans. Dr. Modlin’s research laboratory has made fundamental insights into T-cell subsets, cytokine patterns, antigen presentation, innate immunity and antimicrobial mechanisms in the human immune response to infection. He has been awarded three patents for this research and has published more than 180 articles, including 13 papers in Science and Nature, and 4 in Nature Medicine. The Modlin lab's manuscript identifying distinct T cell cytokine profiles in leprosy lesions has been cited more than 1,000 times. An exciting recent discovery is the elucidation of the mechanism by which vitamin D subsets contributes to innate immunity against tuberculosis in humans, providing a rationale for therapeutic intervention.

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Dr Rasmus Mortensen


Dr. Mortensen received his doctorate in immunology and vaccinology at University of Copenhagen and is now the Head of preclinical TB vaccine development at Statens Serum Institut in Copenhagen, Denmark. His responsibilities cover development activities from early discovery and vaccine design to testing and transitioning into clinical trials. His group is studying protective immunological mechanisms of vaccine mediated immunity and utilize the knowledge gathered in clinical trails and animal experiments to generate better next-generation TB vaccines.

Dr Kevin B. Urdahl, MD, PhD


​Associate Professor, Center for Infectious Disease Research
Affiliate Associate Professor, Immunology
Clinical Associate Professor, Pediatrics
University of Washington

Dr. Urdahl graduated from Concordia College (Moorhead, Minnesota), and earned an MD and a PhD in Microbiology/Immunology from the University of Minnesota. He completed a Pediatrics residency and an Infectious Diseases fellowship at Seattle Children’s Hospital, and his postdoctoral work in Immunology at the University of Washington. He started his career as a primary investigator in the Department of Pediatrics at the University of Washington before joining Seattle Biomedical Research Institute in 2010 (now the Center for Infectious Disease Research). Dr. Urdahl continues to be an attending physician in Pediatric Infectious Diseases at Seattle Children’s Hospital. Dr Urdahl co-leads the T-cell Immunology working group for the Collaboration for TB Vaccine Discovery (CTVD) at the Bill & Melinda Gates Foundation.

​​The Urdahl lab is interested in understanding the factors that impede T cell-mediated immune protection during persistent Mtb infection. We have recently discovered that Foxp3-expressing regulatory T cells (T regs) restrict Mtb eradication, and pathogen-specific T regs are extremely potent in mediating this activity. Even small numbers of Mtb-specific T regs delay the arrival of effector T cells in the lung, the primary site of Mtb infection, and cause an increased bacterial burden. Future research will seek to elucidate how Mtb-specific T regs are induced and to define their precise roles and activities at different stages of infection. A key question that drives these studies is whether T reg function can be safely manipulated to prevent or treat tuberculosis. We are also interested in understanding T cell subsets that promote protection against tuberculosis. Using recently developed MHC class I and II tetramers, we can monitor the function of Mtb-specific CD8+ and CD4+ T cells throughout the course of infection. We seek to determine the lineage relationships between Mtb-specific T cells with different functional capacities, including proliferation, IFN-y production, IL-17 production, and Foxp3 expression. We plan to investigate how variations in innate immune responses help shape the subsequent T cell responses to Mtb. These studies will provide insights into how long-lived populations of protective T cell subsets are induced and maintained during persistent Mtb infection, and should help to inform novel immunization strategies.


Dr Peter Andersen

Dr Cecilia Arlehamn

Dr Sam Behar

Dr Rhea Coler

Dr Mark Davis

​Dr Alistair Leslie

​Dr Deborah Lewinsohn

​Dr Gerhard Walzl