Assistant Professor, Microbiology & Molecular Genetics University of California, Irvine
My group is interested in understanding the impact of genetic variants on the function of immune cells and on predisposition to pathologies driven by the immune system. In particular, we are interested in studying defects of the DNA methylation pathway in the context of aging-associated clonal hematopoiesis. Acquired mutations in DNMT3A (a writer of DNA methylation) and TET2 (an eraser of DNA methylation) are common in the hematopoietic stem cells of elderly individuals, estimated to affect more than 10% of adults over the age of 65. These mutations increase the risk for various age-related comorbidities such as atherosclerosis, thereby nearly doubling the mortality rate of affected individuals. We hypothesize that these mutations impair DNA methylation remodeling that occurs during the differentiation of hematopoietic stem cells, leading to altered gene expression and function of terminally differentiated immune effector cells such as macrophages. We use various cutting-edge human genetic and epigenetic tools and experimental model systems such as human pluripotent stem cell-derived macrophages to address our questions.
Professor of Microbiology and Immunology and the Immunology Program University of Michigan Medical School
My laboratory focuses on investigating on the molecular and cellular mechanisms that govern immune function by T cells. Our recent studies revealed that iron homeostasis is crucial for naïve T cell maintenance by controlling mitochondrial integrity and metabolic programming. We are currently working to understand the underlying mechanisms.
Professor, Biomedical Sciences Iowa State University
Development of a vaccine against human immunodeficiency virus (HIV-1), the virus that causes AIDS. In connection with this research, we characterize biochemical and immunological properties of viral envelope glycoprotein, develop and evaluate novel vaccine vectors, and examine virus-host interactions at various levels.
Associate Professor of Dermatology (Medical Dermatology) and Biochemistry and Molecular Genetics at Northwestern University
Our lab studies T cell biology. We employ cutting-edge genomics approaches to elucidate the role of T cells in immunohomeostasis and disease. We apply this knowledge to elucidate the cellular players and molecular circuitry that drive pathological changes in the skin in diseases such as skin cancer, cancer of skin immune cells, and autoimmune disease. Currently, there is an unprecedented opportunity to study and modify T cells in the setting of disease. The goal is to translate these findings to clinical trials.
Professor, Pathology & Immunology Washington University in St. Louis, School of Medicine
Hematopoietic and endothelial development We study hematopoietic and endothelial cell development. We focus on the molecular mechanisms that control mesoderm commitment to the hematopoietic and endothelial cell lineages. Particularly, we investigate the interaction among VEGF, Flk1, and an ETS transcription factor ETV2, as these three factors play a deterministic role in the formation of hematopoietic and endothelial cells. We have expertise in hematopoietic, vascular, and stem cell biology and stem cell applications. Hematopoiesis and angiogenesis in cancer We study hematopoiesis and angiogenesis in the context of cancer. Particularly, we investigate mechanisms that lead to hematopoietic stem and progenitor changes in the tumor. We also investigate mechanisms by which tumor angiogenesis affects tumor immunity. We hope to apply the knowledge obtained from these studies to ultimately modulate tumor immunity and tumor growth.
Leonard Jarett Professor of Pathology and Laboratory Medicine Perelman School of Medicine, University of Pennsylvania
Dr. Choi's is interested in the molecular analysis of the osteoimmune system. The fields of immunology and bone biology have matured such that key cellular and molecular mechanisms governing the homeostasis of the individual systems are largely understood. However, despite extensive cross-regulation between bone metabolism and the immune system, the mechanisms by which one regulates the other, and the biological implications of such interactions, are poorly understood. ...
Associate Professor, Physiology University of California, Los Angeles
Ca2+ signaling is critical for the function of immune cells. Previously, our group identified Orai1 as the long-sought pore component of the predominant Ca2+ channels in immune cells. In collaboration, we identified patients with a genetic mutation in Orai1 that causes lethal, severe combined immune deficiency. Considering the crucial role of Orai1 in the immune system, understanding of its regulatory mechanism is crucial for development of new therapies targeting diseases caused by hypersensitive immune reaction such as type I diabetes, rheumatoid arthritis, multiple sclerosis, and psoriasis. The main goals of our research are; (i) basic studies to understand the regulatory mechanism of the Orai1-NFAT pathway, (ii) development of animal model systems to test the therapeutic potential of blocking Orai1, and (iii) identification of methods to modulate Orai1 activity to balance the immune system. The developing research areas of interest include; (i) broad understanding of the role of the Orai1-NFAT pathway in various cell types (e.g., stem cells, excitable cells, and innate immune cells), and (ii) elucidation of crosstalk between the Orai1-NFAT pathway and other signaling pathways. These goals will be achieved by various tools including proteomics (large-scale protein purification and mass spec analysis), genome-scale or chemical library high throughput screens, advanced microscopy in live cells, transcriptome analyses, and animal disease models of infection and autoimmunity.
Professor, Molecular Microbiology and Immunology University of Missouri, Columbia
Our research is focused on investigating the mechanisms of RNA virus-host interaction, viral regulation of host immunity, and viral pathogenesis. We create and utilize small-animal models and tissue culture systems for infection with RNA viruses such as influenza virus and lymphocytic choriomeningitis virus (LCMV). Our study should assist in the development of novel therapies including anti-viral drugs and immune therapeutics to remedy diseases caused by viral infections.
Professor, Microbiology, Immunology, and Cancer Biology University of Virginia
My research is focused on elucidating the immunoregulatory mechanism by Hepatitis C virus (HCV). HCV is a global health concern causing severe liver disease such as fibrosis, cirrhosis and hepatocellular carcinoma. HCV infection in humans is remarkably efficient in establishing viral persistence. T cell responses have been reported to play a pivotal role in controlling HCV infection. However, HCV-specific T cell responses are significantly impaired in chronic HCV patients. This suggests that HCV may employ numerous mechanisms to counteract or possibly suppress the host T cell responses. Recent studies in my lab demonstrate that exosomes released from HCV-infected hepatocytes display TGF-beta at the exosome surface and suppress T cell responses. Exosomes are small membrane-bound extracellular vesicles and serve as natural carriers of signaling molecules to promote cellular crosstalk. We are currently studying to identify the cellular and molecular mechanism for the role of exosomes released from HCV-infected hepatocytes in regulating the host immunity and promoting the development of liver fibrosis. A better understanding of HCV-mediated immune regulation will provide a rational basis for immunotherapeutic strategies to prevent chronic HCV infection and chronic liver diseases.
Dr. Han's research programs focus on 1) The role of RNA-binding proteins and non-coding RNAs in cancer development and progression, 2) Ovarian and Lung cancer initiation and progression, 3) Developing novel therapeutic strategies for cancer based on cancer genomics and metabolomics.
Associate Professor of Immunology Harvard Medical School
My laboratory has previously discovered a critical pathway linking gut bacterial species to an inflammatory cascade that ultimately leads to behavioral abnormalities including deficit in social behaviors. Remarkably, this communication between the gut and the brain occurs during prenatal development and has a very specific effect: the bacteria that drive the inflammation reside in the maternal gut, and lead to the aberrant development of a sub-region of the primary somatosensory cortex. This work is one of the first studies to describe a mechanistic pathway linking the gut-immune-brain axis. Ongoing work in the lab focuses on a particular class of immune cells called Th17 cells to determine if these cells and the signals they produce drive the observed inflammation-induced abnormal behavioral phenotypes. To this end, we have found that some of the signals released by Th17 cells have receptors in the fetal brain and this might be the route through which the immune system directly impact the brain. We are also trying to elucidate mechanisms by which host- and bacteria-derived small molecules modulate inflammation and how they affect neural activity and animal behaviors.
Professor, Department of Biological Chemistry and Molecular Pharmacology Harvard Medical School
Our laboratory investigates the molecular mechanisms of the vertebrate immune system. We are particularly interested in protein aggregates, namely “functional aggregates”, that play increasingly important and common functions in immune systems. Our interest in functional aggregates started with our investigation of the innate immune receptors, RIG-I-like receptors, which recognize viral RNAs during infection and activate the antiviral immune response. We discovered that RIG-I-like receptors and their downstream signaling molecules assemble into higher order oligomers (i.e. filaments) during viral RNA detection and signal transduction. We additionally showed that their functions depend upon tightly controlled assembly and disassembly processes to prevent aberrant protein oligomerization/aggregation and immune activation. These findings have also led us to explore other functional aggregates in different biological contexts, such as transcriptional regulation in the adaptive immune system. ...
Assistant Professor, Dept. of Stem Cell Transplantation and Cellular Therapy The University of Texas MD Anderson Cancer Center
My research is focused on investigating CD1 antigen presenting system and CD!-restricted T cells in immune-regulation, More recently, we have been investigating the role of CD1d-restricted invariant Natural Killer (iNK) T cells in immune-regulation post allogeneic stem cell transplantation through translational approach, and developing novel cellular therapy using ex vivo expanded iNK T cells to prevent Graft Versus Host Disease (GVHD) using murine xenograft GVHD model. We will further enhance Graft Versus Leukemic effect of iNK T cells targeting tumor antigens using genetic modification with chimeric antigen receptors. Our research strategy involves various methods commonly employed in immunology research, ranging from basic molecular and cellular immunology to in vivo animal studies, not limiting to molecular cloning, protein expression, novel NGS-based single T cell transcriptome analysis, multi-color flow cytometry etc.
Betsy deWindt Professor, Chair of Cancer Biology Department, Director of Infection Biology Program and Director of Global Center for Pathogen Research and Human Health at Lerner Research Institute, Cleveland Clinic
My research is divided into four areas: (1) virus-induced cancer (gamma-2 herpesvirus and hepatitis B virus); (2) emerging virus: mosquito-borne flavivirus (Dengue virus and Zika virus), tick-borne bunyavirus (Severe Fever with Thrombocytopenia virus and Heartland virus) and air-borne virus (severe acute respiratory syndrome coronavirus 2 and influenza virus); (3) therapeutic and vaccine development and stabilization, and (4) inflammation and immunity (host-pathogen standoff, programmed cell death, immune atlas of pregnancy and inflammation). The overarching goal of my research is to uncover new ways to understand infection and immunity and to rapidly develop and distribute vaccines and therapeutics to improve global health.
Professor; Director of Allergy & Immunology, Internal Medicine Yale School of Medicine
Dr. Insoo Kang is Professor of Medicine (Rheumatology, Allergy & Immunology) at Yale University School of Medicine. He completed his post-graduate training in rheumatology and immunology research at Yale. He has been on the faculty at Yale School of Medicine since 1999. He is a physician scientist with a research interest in understanding the human immune system using biological samples and clinical data. In particular, Dr. Kang has defined subsets of T cells with distinct cellular characteristics based on the expression of cytokine receptors on T cells in health and disease as well as the interactions of such cell subsets with monocytes and other immune cells.
Lymphocytes guard against pathogens to maintain an organism’s integrity and health. However, there are some costs to this protection. Lymphocytes are prone to transformation, and leukemia and lymphomas can arise. Lymphocytes can also cause harm to self, and the frequency of autoimmune disease is increasing alarmingly in developed western nations, which comes with immense social costs. By understanding how these diseases develop we can formulate new, specific therapies that will have minimal side effects. Conversely, new drugs that can hyperactivate T cells may enhance efficacy of T cell immunotherpies against cancer. In our lab, we study the normal process of T lymphocyte development to understand how and why things go wrong. We are also exploring how T cells function to maintain tolerance to self, poised to react only to disease-causing foreign pathogens and to survery for cancer cells.
Professor, Institute for Biomedical Sciences Georgia State University
Research Interest: Design of vaccines based on mRNA genetic and recombinant protein platforms. Developing effective vaccines against respiratory viruses: Influenza Virus, SARS-CoV-2 (COVID-19), Human Respiratory Syncytial Virus (RSV). Understanding protective immune responses of vaccination.
Kenneth and Judy Betz Family Endowed Professor of Pathology University of Michigan
Kim Lab has made many seminal discoveries in lymphocyte biology and mucosal immunology. Key discoveries made by Dr Kim and his collaborators include: 1) chemoattractant gradients across the bone marrow and peripheral blood circulation for stem cell homing (1997-2006), 2) intrathymic chemotactic migration of developing thymocytes (1998-2000); 3) Identification of chemokine receptors for polarized effector or regulatory T cells (Th1, Th2, Th17 and Tregs) (2000-2011); 4) germinal center-residing B cell-helping Tfh cells (1999-2005); 5) Tfr cells and their function in suppressing B cells (2003-2005);
More recent contributions include 6) roles of nuclear hormone receptor ligands (e.g. retinoic acid) in inducing Tregs and immune tolerance through multiple mechanisms (2006-present); 7) the role of short-chain fatty acid (SCFA) receptors in regulating the barrier immune function of intestinal epithelial cells (2011-present); 8) gut-homing mechanisms for innate lymphoid cells (ILC) subsets (2013-present); 9) roles of the microbial metabolites SCFAs in generating Tregs, effector T cells, and plasma B cells (2011-present).
Associate Professor of Radiology Northwestern University
My research has been focused on therapeutic carriers for treatment of various types of cancer. Micro/Nanoparticles and their hybrid derivatives have been exploited as vectors for drug delivery, hyperthermia, cell therapy, immunotherapy and as molecular imaging agents of MRI, CT, ultrasound and fluorescents. Currently working closely with clinicians, medical scientists, biologist and imaging professionals to translate new cancer therapeutic approaches using multifunctional carriers and diagnostic imaging technique to the clinical setting.
Sol and Clara Kest Professor of Dermatology Icahn School of Medicine at Mount Sinai
The Kim Lab has unique expertise in basic approaches and techniques in innate immunity, neuroimmunology, and behavioral modelling of chronic itch. Therefore, we are able to provide state of the art guidance on in vitro, ex vivo, and in vivo experimental systems to better understand skin immunity, inflammation, and sensation.
ASSISTANT PROFESSOR OF PHARMACOLOGY University of Illinois at Chicago
Our lab investigates development and physiological roles of mononuclear phagocytes in steady state as well as pathological conditions (both inflammatory phase and resolving-phase) taking advantage of cutting-edge lineage-tracing approaches, cell ablation strategy and in-vivo imaging techniques combined with high throughput transcriptomic analysis. Specifically, we focus on (1) roles of two monocyte populations (Ly6Chi CX3CR1int and Ly6Clo CX3CR1hi subsets) in either promoting or resolving the inflammation, (2) transition of monocytes to macrophage/dendritic cells and their impact on inflammation/ tissue repair, and (3) distinct roles of embryonic-derived macrophages and monocyte-derived macrophages in a variety of physiological or pathological conditions.
Professor of Department of Microbiology and Immunology University of Rochester Medical Center
Precise spatial and temporal regulation of cell migration is critical not only for normal immune responses, but also for successful organ development, wound healing, and tumor metastasis. Integrins, a family of membrane receptors, are expressed in all different types of cells in human body and regulate important cell adhesion and migration. Early in his career, Dr. Kim developed a highly innovative bio-imaging assay using FRET (Fluorescence Resonance Energy Transfer) techniques and show for the first time in live cells that the intracellular domains of integrin LFA-1 moved apart substantially during immune cell migration, and his paper describing this (Kim et al. 2003, Science) has been highly cited and is regarded as a cornerstone of the integrin field. Dr. Kim has continued to develop this area in his lab in Rochester, establishing a role for conformational change in other important integrins like Mac-1 and VLA-4.
Assistant Professor of Department of Microbiology and Immunology Thomas Jefferson University
Our focus is to study how immune homeostasis in non-lymphoid tissue (such as mucosal area) is accomplished by T cells and what is the role of local environment (such as gut microbiota) in that process. With intestine as a model system, we will study how T cells migrate there, what type of antigens local T cells recognize, and what is the contribution of those local T cells in the gut immune responses.
Associate Professor, Institute of Molecular Medicine Feinstein Institutes for Medical Research
The focus of Dr. Kim’s laboratory research is to identify the regulatory mechanism of inflammatory function of dendritic cells under both homeostatic and inflammatory conditions. To understand the molecular mechanisms underlying inhibition of development of autoimmune diseases, particularly in systemic lupus and inflammatory bowel diseases, we are using an animal model of SLE which has a dendritic specific deletion of transcription factor, Blimp-1.
Associate Professor, Medical Microbiology and Immunology University of California, Davis
Innate immune responses to viral infection and malignancy, Development and function of natural killer cells in humans and animal models, Non-human primate model of viral infection.
Assistant PROFESSOR, DEPARTMENT OF MEDICINE/PATHOLOGY, MOLECULAR MICROBIOLOGY AND IMMUNOLOGY VANDERBILT University
1. Overcoming immune evasion in leukemia 2. Dissect graft-versus-host disease and graft-versus-leukemia in allogeneic stem cell transplantation (allo-SCT) by manipulating co-inhibitory molecules 3. Human correlative studies in line with clinical trials
PROFESSOR, DEPARTMENT OF MOLECULAR MICROBIOLOGY AND IMMUNOLOGY Brown University
My role in basic and clinical research has largely derived from my position as Director of the Molecular Biology Core in the Section of Pulmonary Medicine. In that capacity, I have generated and characterized lung-specific overexpressing transgenic and null mutant mice to study in vivo roles and the effect of various cytokines in the pathogenesis of asthma, acute lung injury, pulmonary vascular disease, pulmonary fibrosis and emphysema.
Associate Professor, Department of Medicine Emory University
As a pulmonary immunologist, her research focus is in understanding the biology of human plasma cells in health and disease in bone marrow, blood, and respiratory tissues. Recently, her laboratory has identified a unique phenotype of human long-lived plasma cells (LLPC) in the bone marrow, and she is interested in understanding the mechanisms of how LLPC are generated and maintained. Another part of her laboratory focuses on the human plasmablasts/antibody secreting cells (ASC) that circulate during an active immune response such as vaccination or infection. They have proof of concept demonstrating that the ASCs in the blood during illness are informative in identifying the pathogen causing illness. This novel approach is the basis of a new immune-diagnostic platform. Finally, tying her clinical interests in asthma and allergy, she is also interested in studying the biology of the plasma cells in upper and lower respiratory tract with primary focus on IgE plasma cells.
Assistant Professor, Department of Biochemistry & Molecular Biology University of Calgary
The ability of immune cells to target cancer cells has revolutionized cancer treatments. Adoptive cellular therapy (ACT) directly utilizes immune cells to treat cancers as living drugs and offers promising treatment strategies for some patients with no alternative options. Dr. Jongbok Lee’s research focuses on developing novel ACT using a subset of immune cells called double-negative T cells (DNT).
Professor, President of Soonchunhyang Institute of Medi-bio Science (SIMS) Soonchunhyang University
Lee lab has been studying the underlying molecular mechanisms for the development of obesity-induced insulin resistance, especially focusing on investigating how immune cells are regulated by obesity and how these then mediate the development of obesity-induced systemic insulin resistance. The current research projects of Lee lab are on 1) assessing the metabolic functions of adipose tissue macrophages, 2) determining the role of adipose tissue NK cells in the development of obesity-induced inflammation and insulin resistance, and 3) investigating the molecular mechanisms how adipose tissue inflammation regulates insulin resistance in the liver, muscle and β-cells.
Professor, Dept. of Biochemistry, Microbiology, and Immunology The University of Ottawa
Research Interests: My lab focuses on important questions involving natural killer (NK) cells with two major research themes: (1) Identification of novel NK cell functions and dissection of mechanisms for those functions in vivo in models of infection and cancer; (2) Application of these new findings for developing innovative therapeutics. We have established a network of collaborations with clinical investigators in order to elucidate new NK cell functions of relevance to cancer therapy and the treatment of chronic infections.
Assistant Professor, Department of Pediatrics Emory University School of Medicine
Dr. Sujin Lee received her PhD in Viral Immunology from University of Tennessee. Her research interests are respiratory syncytial virus (RSV) vaccine and T-cell immune responses to pathogens. Her current focus is the development of peptide-based vaccine using CD8 and CD4 epitopes with Toll-like receptor (TLR) agonists as adjuvants. Also, she is studying the host immune response to RSV vaccination in the settings of immunocompetence and immunosenescence using a mouse model of aging. Her ultimate goals are 1) to understand the underlying mechanisms how immune responses are regulated by RSV infection or vaccination, 2) to generate the most efficient protective memory immune responses, 3) to define the role of helper T cells in the regulation of cytotoxic T cell responses to RSV antigens, and 4) to establish a basis for a novel vaccine strategy against RSV to make RSV vaccines to prevent RSV disease.
Associate Professor, Department of Microbiology Icahn School of Medicine at Mount Sinai
Dr. Lim completed her postdoctoral training at the National Institutes of Health in 2010 after receiving her Ph.D. in Microbiology and Immunology from the University of Maryland, School of Medicine. Throughout her career, she has focused primarily on understanding the host response to viral infections, with a focus on understanding the impact of inflammatory responses on viral pathogenesis. In 2010, Dr. Lim joined the team of virologists at the Icahn School of Medicine, where she currently studies the pathogenesis of viral infections as an Associate Professor in the Department of Microbiology.
Professor of Microbiology-Immunology Northwestern University
The immune system is tightly controlled by multiple mechanisms, and Foxp3+ regulatory T (Treg) cells are prominent active regulators of immunity and tolerance. Defects in Treg cell generation or function result in uncontrolled systemic autoimmune inflammation. Despite extensive investigation in Treg cell biology, our understanding the mechanisms underlying Treg cell development and functions still remains incomplete. There is increasing evidence that Treg cell functions can be compromised under certain conditions, and such dysregulation is thought to be a contributing factor of chronic inflammatory conditions. Our laboratory studies both cellular and molecular factors that control Treg cell functions.
J. G. Searle Professor, Pharmaceutical Sciences University of Michigan, Ann Arbor
The immune system is tightly controlled by multiple mechanisms, and Foxp3+ regulatory T (Treg) cells are prominent active regulators of immunity and tolerance. Defects in Treg cell generation or function result in uncontrolled systemic autoimmune inflammation. Despite extensive investigation in Treg cell biology, our understanding the mechanisms underlying Treg cell development and functions still remains incomplete. There is increasing evidence that Treg cell functions can be compromised under certain conditions, and such dysregulation is thought to be a contributing factor of chronic inflammatory conditions. Our laboratory studies both cellular and molecular factors that control Treg cell functions.
Professor - Emeritus (P), Department of Medicine The University of Alabama at Birmingham
Moon H. Nahm, Professor of Department of Medicine, with secondary appointment in Microbiology, obtained both his BA degree (in 1970) and MD degree (in 1974) from Washington University in St. Louis MO. In 1980, he completed both Internal Medicine and Laboratory Medicine residency training in Pathology Department, as well as completing post-doctoral research training in Microbiology Department at Washington University in St. Louis MO. He was a faculty member at Washington University in St. Louis and University of Rochester before he joined UAB. He was the director of the Clinical Immunology Laboratory for UAB hospitals.
● Currently managing novel immune-oncology pipeline projects in Amgen as a project team leader. ● Established cancer immunology and immunology scientist with deep cutting-edge understanding in both fields. ● Critical thinking and scientific excellence in innovation proven by the track records of project development, first author publications in top-tier immunology journals, invited oral presentations in prestigious conferences, patent application, and award winnings.
Professor of Medicine University of Illinois, College of Medicine
Our lab has investigated molecular and cellular mechanisms of immune cells with a more holistic understanding of how these mechanisms work in actual patients. Our studies adopt translational tools based on human samples and apply the data to animal models relevant to human diseases. This approach has resulted in a number of high-quality publications on the phenotypic heterogeneity of immune cells and their transcriptional and posttranslational gene regulation, eventually showing how they modulate pulmonary diseases. More recently, this work has led to an interest in the cellular heterogeneity of macrophages and dendritic cells in asthma. Our lab established the techniques required to analyze the phenotypes and genotypes of innate immune cells, including flow cytometry, sc-RNA-seq, and mass cytometry (CyTOF). To evaluate the clinical relevance of the data from animal models, we run the IRB-approved human translational protocol for bronchoscopic provocation with the sensitized allergen. With the network of collaborators both inside the campus and beyond, our lab will continue to focus on immune cell biology in the lung to understand human lung diseases better.
A. The role of cytokines in immune cell homeostasis under resting and immune activating conditions. Different cell populations occupy different niches for homeostasis. Hence, naive and memory T cells don't compete with each other for limiting resources such as pro-survival cytokines. Whether such niches are privileged sites even to immune activated cells is not clear. In fact, how naive and memory T cell homeostasis works under disease conditions, where large numbers of cells are activated and proliferating, remains to be unraveled. In a previous study (Immunity (2004) 21:289-302), we showed that inflammatory cytokines such as IL-2, IL-4 and IL-6 suppress the transcription and expression of IL-7 receptors. Furthermore, we predicted that such a mechanism would downregulate IL-7 receptor expression on activated T cells thus effectively removing them from the naive T cell pool and out of competition for IL-7-mediated survival signals. ...
• Immunologist in Drug Discovery Research in the field of Cancer Immunotherapy and Inflammatory autoimmune diseases • Project leader for multiple Target Discovery Programs in Immuno-oncology and Inflammatory autoimmune diseases • Leading Translational Research with academic collaborators to determine endotypes of COPD and discover biomarkers for respiratory inflammation through immunophenotyping, nasal RNA-Seq, and single-cell RNA-seq
Associate Professor, Department of Microbiology & Molecular Genetics Michigan State University
Human papillomaviruses (HPVs) are highly prevalent and potent human pathogens that cause over 5% of all human cancers, including cervical cancer (CxCa) and a subset of head and neck cancers (HNC). HPV-associated cancers result in a half of a million deaths every year worldwide. Our research group focuses on investigating virus-host interactions, particularly in the context of host immunity, to develop effective preventive and therapeutic strategies for HPV-associated cancers.
Associate Professor, Department of Medicine UMass Chan Medical School
Bone mass reflects the coupled balance of activity of osteoblasts to synthesize and osteoclasts to degrade bone matrix. Coupling of the activity between these two lineages is required for balance in bone remodeling, and dysregulation of this process is a major mechanism in the pathogenesis of many of human skeletal disorders, such as osteoporosis, inflammation-induced bone loss, and periodontitis. Additionally, osteoblast differentiation capacity of skeletal stem cells must be tightly controlled, as inadequate bone formation results in low bone mass, skeletal fragility, and bone healing defect, while over-exuberant osteogenesis results in extra-bone formation in the soft connective tissues, such as trauma-induced heterotopic ossification and fibrodysplasia ossificans progressiva by a genetic mutation.
Assoc. Professor, Department of Microbiology and Immunology University of California, San Francisco
Dendritic cells play important roles in inducing immunity against microbial antigens while developing tolerance against self or innocuous foreign antigens. Our laboratory is interested in identifying the specific mechanism by which dendritic cells mediate regulatory T cell (Treg) development and defining the biological impact that dendritic cells make on immune suppressive function of Treg. Our recent study implicates the role of Membrane-Associated RING finger CH 1 (MARCH1) ubiquitin ligase in dendritic cell selection of natural Treg. Current research focuses on defining the molecular mechanism by which MARCH1 mediates Treg development and determining functional specialization of Treg generated in this MARCH1-dependent manner.
Director, Immune Regulation Research Unit IRCM Research Professor
T cells play a central role in shaping the adaptive immune system. Against non-self antigens with pathogenic threat, T cells should develop immunity. On the other hand, T cells are supposed to become tolerant to self antigens or innocuous environmental antigens. Many immunological disorders such as immunodeficiency, autoimmune diseases, and allergies are caused by T cells that fail to obey the above rules. Members of the CD28 family cosignaling receptors and their ligands (members of B7 family) are known to play crucial roles in T cell immunity and tolerance. The Immune Regulation Research Unit's team is investigating the molecular and cellular mechanisms of CD28-B7 family of T cell cosignaling molecules using a panel of knockout, knockin, and transgenic mice. Impacts of altered T cell cosignaling are analyzed at the biochemical and cellular levels using immune cells isolated from the mice. The consequences of altered cosignaling in overall immune reactions in mice are examined in the context of infection, cancer, and autoimmunity.
The Sung lab applies quantitative imaging, mathematical, epigenomics approaches towards understanding the mechanisms of transcription factor signaling and functional genome regulation. They developed fluorescent knock-in mice that track the canonical subunits of NF-κB (Rahman SMT et al. Cell Reports, 2022) to enable diverse analyses, ranging from single-molecule analyses to in situ identification of active inflammatory cells.
Professor, Dept. of Microbiology, Immunology and Biochemistry The University of Tennessee Health Science Center
Research Interests: Research focuses on identifying new signaling components in host pattern recognition reeceptor and signaling pathways that amplify or attenuate pro-inflammatory responses during the course of infection and autoimmune process.