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[ PhD Program: Immunology Keyword: ]

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NameEmailPhd ProgramResearch InterestsPublications
Ainslie, Kristy M email , , , publications

We have several areas of research interest broadly in the area of immunomodulation using micro/nanoparticles and other carrier systems.  This can include development of traditional vaccines, therapeutic autoimmune vaccines and classic drug delivery platforms targeted to bacterial, viral or parasitic host cells.  To this end, we also seek to develop new materials and platforms optimal for use in modulating immune responses as well as developing scalable production of micro/nanoparticles.

Arthur, Janelle C. email , , , , publications

The Arthur lab is interested in mechanisms by which inflammation alters the functional capabilities of the microbiota, with the long-term goal of targeting resident microbes as a preventative and therapeutic strategy to lessen inflammation and reduce the risk of colorectal cancer. We utilize a unique and powerful in vivo system – germ-free and gnotobiotic mice – to causally link specific microbes, microbial genes, and microbial metabolites with health and disease in the gut.  We also employ basic immunology and molecular microbiology techniques as well as next generation sequencing and bioinformatics to evaluate these essential host-microbe interactions.

Beck, Melinda A. email , , publications

My laboratory studies the relationship between host nutrition and the immune response to infectious disease. Using a mouse model of obesity, we are exploring the mechanism(s) for high mortality from influenza infection in obese mice compared with lean mice. We also have an ongoing clinical research study designed to understand the mechanism(s) involved that impair the influenza vaccine response in obese adults compared with healthy weight adults. We have also demonstrated that host deficiencies in antioxidant nutrients can lead to viral mutations resulting in an avirulent pathogen becoming virulent, suggesting that the host nutritional status can be a driving force for the evolution of viruses.

Braunstein, Miriam email , , , , publications

Our research focuses on understanding the virulence mechanisms of Mycobacterium tuberculosis, the bacterium responsible for the disease tuberculosis.

Burks, Wesley email , , , , publications

The UNC Food Allergy Institute (UNCFAI) was established in 2012 to address the growing needs of children and adults with food allergy. Program investigators study the biologic basis of food allergy in the laboratory and in clinical research studies seeking to better understand the role of allergen-specific IgE and the mechanism of allergen immunotherapy. The Institute provides comprehensive, family-centered patient care for food allergy, food-related anaphylaxis, and other related disorders like atopic dermatitis and eosinophilic esophagitis.

Cairns, Bruce A. email , , , , publications

The immune system of severely burned patients becomes extremely suppressed after injury. An overwhelming number of patients die from wound infection and sepsis. However, we are unable to graft these patients with skin from other donors as their immune system is still able to reject the graft efficiently. Our inability to cover the wound site leaves the patients further open to bacterial and fungal infections. Our laboratory investigates the translational immune mechanisms for these devastating consequences of burn within mouse models and burn patients. Focuses in the lab include  1) investigation of innate molecule control of both the innate and adaptive immune systems after burn injury, 2) Role of innate signaling to Damage Associated Molecular Patterns in Immune Dysfunction after burn / inhalational injury,focusing on  mTOR-mediated Immunomodulation 3) Using NRF2/KEAP1-Targeted Therapy to Prevent Pneumonitis and Immune Dysfunction After Radiation or Combined Burn-Radiation Injury and 4) Investigating sex-specific disparities in Immune Dysfunction after trauma / transplantation. ​

Chen, Xian email , , , , publications

Developing and applying novel mass spectrometry (MS)-based proteomics methodologies for high throughput identification, quantification, and characterization of the pathologically relevant changes in protein expression, post-translational modifications (PTMs), and protein-protein interactions.  Focuses in the lab include: 1) technology development for comprehensive and quantitative proteomic analysis, 2) investigation of systems regulation in toll-like receptor-mediated pathogenesis and 3) proteomic-based mechanistic investigation of stress-induced cellular responses/effects in cancer pathogenesis.

Darville, Lee Antoinette (Toni) email , , , , publications

Research in the Darville lab is focused on increasing our understanding of immune signaling pathways active in development of genital tract disease due to Chlamydia trachomatis and determination of chlamydial antigen-specific T cell responses that lead to protection from infection and disease. In vitro, murine model, and human studies are being performed with the ultimate goal to develop a vaccine against this prevalent sexually transmitted bacterial pathogen. Genetic and transcriptional microarray studies are being performed to explore pathogenic mechanisms and determine biomarkers of pelvic inflammatory disease due to Chlamydia as well as other sexually transmitted pathogens.

De Paris, Kristina email , , , publications

Our research focuses on the immunological aspects of pathogen-host interactions. The lab is actively involved in HIV pathogenesis and vaccine studies using the nonhuman primate model of SIV infection. We are particularly interested in pediatric HIV transmission by breast-feeding and the early, local host immune response. A main research focus is on developmental differences in host immune responses between infants and adults and how they alter pathogenesis. The effect of co-infections (e.g. malaria and Tb) on HIV pathogenesis and transmission is a second research focus. The lab is developing a nonhuman primate model of SIV-Plasmodium fragile co-infection to study HIV-P. falciparum infection in humans.

de Silva, Aravinda email , , , , publications

We study Borrelia burgdorferi (the agent of Lyme disease) as a model for understanding arthropod vector-borne disease transmission. We also study the epidemiology and pathogenesis of dengue viruses associated with hemorrhagic disease.

Diaz-Sanchez, David email , , , , publications

The work focuses on how air pollutants affect human health, the role of genetics and epigenetic factors in determining susceptibility and clinical/dietary strategies to mitigate these effects. There is a strong emphasis on translational research projects using a multi-disciplinary approach. Thus, by using human in vivo models (such as clinical studies) we validate in vitro, epidemiology, and animal findings.

Doerschuk, Claire M email , , , , publications

We study host defense mechanisms in the lungs, particularly the inflammatory and innate immune processes important in the pathogenesis and course of bacterial pneumonia, acute lung injury/acute respiratory distress syndrome, and cigarette smoke-associated lung disease. Basic and translational studies address mechanisms of host defense, including recruitment and function of leukocytes, vascular permeability leading to edema, bacterial clearance and resolution.  Cell signaling pathways initiated by binding of leukocyte-endothelial cell adhesion molecules and molecular mechanisms underlying the functions of neutrophils are two particular areas.

Duncan, Alex email , , , , publications

My lab studies a recently identified pathogen-sensing signaling complex known as the inflammasome. The inflammasome is responsible for the proteolytic maturation of some cytokines and induces a novel necrotic cell death program. We have found that critical virulence factors from certain pathogens are able to activate NLRP3-mediated signaling, suggesting these pathogens may exploit this host signaling system in order to promote infections.  Our lab has active research projects in several areas relating to inflammasome signaling ranging from understanding basic molecular mechanisms of the pathway to studying the role of the system in animal models of infectious diseases.

Fessler, Michael B. email , , , publications

Fessler laboratory investigates mechanisms of the innate immune response, in particular Toll like Receptor (TLR) pathways and how they regulate inflammatory and host defense responses in the lung.  To this end, we use both in vitro (macrophage cultures) and in vivo (mouse models of acute lung injury and pneumonia) model systems, and also use translational approaches (e.g., studies using human peripheral blood leukocytes and alveolar macrophages).  An area of particular interest within the laboratory is defining how cholesterol trafficking and dyslipidemia innate immunity.

Garcia-Martinez, J. Victor email , , , , publications

Over millions of years of coexistence humans and pathogens have develop intricate and very intimate relationships.  These highly specialized interactions are the basic determinants of pathogenesis and disease progression.  Our laboratory is interested in elucidating the molecular basis of disease.  Our multidisciplinary approach to molecular medicine is based on our interest in the translation of basic research observations into clinical implementation.  For this purpose we use a variety of in vitro and in vivo approaches to study AIDS, Cancer, immunological diseases, gene therapy, etc.  Of particular interest is the use of state of the art models such as humanized mice to study human specific pathogens like HIV, EBV, Kaposiâ’s sarcoma, influenza, xenotropic murine leukemia virus-related virus.  In addition, we are interested in the development and implementation of novel approaches to prevent viral transmission using pre-expossure prophylaxis and vaccines.

Gilmour, M Ian email , , , , publications

Dr M Ian Gilmour is a Principal Investigator at the National Health and Environmental Effects Research Laboratory (NHEERL), U.S Environmental Protection Agency in RTP.    He received an Honors degree in microbiology from the University of Glasgow, and a doctorate in aerosol science and mucosal immunology from the University of Bristol in 1988.  After post-doctoral work at the John Hopkins School of Public Health and the U.S. EPA, he became a Research Associate in the Center for Environmental Medicine at the University of North Carolina. In 1998 he joined the EPA fellowship program and in 2000 became a permanent staff member.  He holds adjunct faculty positions with the UNC School of Public Health and the Curriculum in Toxicology, and at NC State Veterinary School.  He has published over 80 research articles in the field of pulmonary immunobiology where his research focuses on the interaction between air pollutant exposure and the development of infectious and allergic lung disease.

Goldman, William email , , , , publications

Successful respiratory pathogens must be able to respond swiftly to a wide array of sophisticated defense mechanisms in the mammalian lung.  In histoplasmosis, macrophages — a first line of defense in the lower respiratory tract — are effectively parasitized by Histoplasma capsulatum.  We are studying this process by focusing on virulence factors produced as this “dimorphic” fungus undergoes a temperature-triggered conversion from a saprophytic mold form to a parasitic yeast form.  Yersinia pestis also displays two temperature-regulated lifestyles, depending on whether it is colonizing a flea or mammalian host.  Inhalation by humans leads to a rapid and overwhelming disease, and we are trying to understand the development of pneumonic plague by studying genes that are activated during the stages of pulmonary colonization.

Goonetilleke, Nilu email , , publications

We are a human immunology lab focusing on all aspects of T cell immunobiology in HIV-1 infection. Studies range from basic questions like, ‘What are the determinants of the first T cell response following infection?’ to translational challenges such as ‘What is the best design for a T cell vaccine to either prevent infection or achieve HIV-1 cure?’

Keywords: T cells, HIV-1, Escape, CD8 T cells, Vaccines, Cure, Vaccines

Hansen, Jonathan email , , , publications

Current research indicates that inflammatory bowel diseases (IBD’s), including Crohn’s disease and ulcerative colitis, are due to uncontrolled innate and adaptive immune responses to commensal (non-pathogenic) intestinal bacteria in genetically susceptible hosts.  However, the roles of intestinal bacteria in the perpetuation and progression of IBD’s are unclear and the effects of intestinal inflammation on commensal bacterial physiology and virulence are unknown.  We hypothesize that commensal bacteria dynamically respond to intestinal inflammation in a manner that perpetuates or worsens disease.  Exploring this hypothesis will enhance our understanding of the pathogenesis of IBD’s and host-microbial interactions, and potentially identify new therapeutic targets for these currently incurable diseases.

Heise, Mark email , , , , , publications

We study alphavirus infection to model virus-induced disease.  Projects include 1) mapping viral determinants involved in encephalitis, and 2) using a mouse model of virus-induced arthritis to identify viral and host factors associated with disease.

Homeister, Jonathon W. email , , , , publications

Our research focuses on understanding the molecular and cellular mechanisms of leukocyte (white blood cell) trafficking and homing in vascular inflammation and immune responses. We are interested in the glycobiology of the Selectin leukocyte adhesion molecules and their ligands, and understanding the roles for these glycoproteins in the pathogenesis of inflammatory/immune cardiovascular diseases such as atherosclerosis and vasculitis. We are also interested in the mechanisms whereby the selectins and their ligands link the inflammatory response and coagulation cascade and thereby modulate thrombosis and hemostasis.

Jaspers, Ilona email , , , , , publications

Research in my lab focuses on the mechanisms by which exposure to air pollutants alters respiratory immune responses and modifies susceptibility to and the severity of respiratory virus infections. Specifically, we are examining the effects of air pollutants such as ozone, woodsmoke and tobacco product exposures on host defense responses and influenza virus infections, using several in vitro models of the respiratory epithelium. In collaboration with physician scientists, we are also translating these studies into humans in vivo.

Jennette, Charles J. email , , publications

My research interests and diagnostic responsibilities center around nephropathology and immunopathology. My laboratory carries out basic, translational and clinicopathologic research on kidney diseases. I am most interested in pathogenic mechanisms and pathologic manifestations of glomerular diseases and vasculitis. A major current research focus is on elucidating the pathogenesis of vascular inflammation caused by anti-neutrophil cytoplasmic autoantibodies (ANCA).

Kleeberger, Steven email , , , , publications

Genetic determinants of environmental lung diseases.

Lai, Samuel email , , , , , , , , publications

Our dynamic group are broadly involve in three topics: (i) prevention of infectious diseases by harnessing interactions between secreted antibodies and mucus, (ii) immune response to biomaterials, and (iii) targeted delivery of nanomedicine.  Our group was the first to discover that secreted antibodies can interact with mucins to trap pathogens in mucus.  We are now harnessing this approach to engineer improved passive and active immuniation (i.e. vaccines) at mucosal surfaces, as well as understand their interplay with the mucosal microbiome.  We are also studying the adaptive immune response to polymers, including anti-PEG antibodies, and how it might impact the efficacy of PEGylated therapeutics.  Lastly, we are engineering fusion proteins that can guide targeted delivery of nanomedicine to heterogenous tumors and enable personalized medicine.

Lazear, Helen email , , , publications

We use molecular virology approaches and mouse models of infection to understand innate immune mechanisms that control arbovirus pathogenesis (e.g. West Nile, Zika, and La Crosse viruses). Bat flaviviruses have unusual vector/host relationships; understanding the viral and host factors that determine flavivirus host range is important for recognizing potential emerging infections. We are studying the antiviral effects of interferon lambda (IFN-λ) at barrier surfaces, including the blood-brain barrier and the skin. We also use mouse models of atopic dermatitis and herpes simplex virus infection to understand the effects of IFN- λ in the skin. (Accepting rotation students for spring 2016)

Liu, Zhi email , , , , publications

Biochemistry, cell biology, and immunology of skin, immunopathogenesis of autoimmune and inflammatory skin blistering diseases.

Luebke, Robert email , , , , publications

My interests include immunotoxicant modes of action, developmental immunotoxicity, alternative models to screen and prioritize potential immunotoxicants and shared pathways of toxicity/susceptibility across systems and biological levels of complexity.  Recent projects include exploring the relationship between exposure to amphibole asbestos and the reported increases in systemic autoimmune disease in residents of Libby, MT, developing zebrafish-based alternative methods to screen for developmental immunotoxicants, and most recently, the effects of particulate and gaseous air pollutants on innate and acquired resistance to respiratory pathogens.

Lysle, Donald email , publications

Psychoneuroimmunology; the effects of conditioning on lymphocyte reactivity

Maile, Robert email , , , , , publications

An overwhelming number of burn patients die from wound infection and sepsis. Our laboratory, along with Dr Bruce Cairns, investigates translational immune mechanisms within mouse models and burn patients. Focuses in the lab include  1) investigation of innate molecule control of both the innate and adaptive immune systems after burn injury, 2) role of innate signaling to Damage Associated Molecular Patterns in Immune Dysfunction after burn / inhalational injury 3) using NRF2/KEAP1-Targeted Therapy to Prevent Pneumonitis and Immune Dysfunction After Radiation or Combined Burn-Radiation Injury and 4) Investigating sex-specific disparities in Immune Dysfunction

Makowski, Liza email , , , , , , publications

The Makowski lab focuses on substrate metabolism or “immunometabolism” in immune cells such as macrophages and metabolic reprogramming in complex diseases such as obesity, insulin resistance, atherosclerosis, and cancer. We use mouse models, cell culture, and metabolomics to study the interaction between inflammation and nutrient sensitive pathways. Projects in lab are funded by NIH, AHA, and the Mary Kay Foundation.  Core Techniques include:  Glucose, fatty acid, cholesterol trafficking and metabolism using radiotracer biochemical studies. Cellular bioenergetics. Digital Immunohistochemical Analysis

Markovic-Plese, Silva email , , , , , publications

My long-term goal is to understand and therapeutically target the key mechanisms of disease development in patients with multiple sclerosis (MS).  Our research has been focused on the molecular events involved in the initiation of the autoimmune response in MS, and on the mechanisms of action of immunomodulatory therapies for this disabling disease.  Current projects in the laboratory include transcriptional and proteomic profiling of the peripheral blood cells and cerebrospinal fluid obtained from patients in the early phase of the disease, which lead to the discovery of the high levels of IL-11 in the CSF and its high up-regulation in the blood-derived CD4+ T-cells in patients with clinically isolated syndrome (CIS) suggestive of MS. Our center is uniquely positioned to perform the proposed research, having an access to the clinical samples through the integrated clinical and cellular/molecular biology research.

Martinez, Jennifer email , , , , , publications

The focus of the work in the Martinez lab is to examine the non-canonical roles for the autophagy machinery during inflammation.  Our recent work about LC3-associated phagocytosis (LAP) higlights the importance of this non-canonical autophagic process in maintaining tolerance and preventing unwanted autoinflammatory pathologies.

Matsushima, Glenn K email , , , , , , publications

Our laboratory is interested in innate immune responses during injury to the central nervous system and during inflammation during microbial infections.  Our laboratory has a special interest in autoimmune diseases such as multiple sclerosis and systemic lupus erythematosus.  We also are pursuing drug discovery projects targeting receptors that may modulate demyelinating disease and immune responses.  We use molecular, cellular and biochemical approaches both in vitro and in vivo to identify the function of key mediators during pathogenesis.

Miao, Edward A email , , , publications

We study the mechanisms by which innate immunity detects virulence factor activity in pathogenic bacteria. Research focuses on how macrophages detect bacterial type III secretion systems through the inflammasome, which activates Caspase-1, promoting secretion of the cytokines IL-1b and IL-18, as well as pyroptotic cell death. We manipulate bacterial virulence genetically and probe how this alters innate immune detection during infection. This focus joins the fields of microbial pathogenesis and immunology, utilizing the knowledge and tools of both disciplines.

Nagarajan, Uma M email , , , , , publications

Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen that causes Fallopian tube inflammation and subsequent tubal infertility in women.  Our current research interest is to investigate the role of an innate immune responses to chlamydial infection and its role in genital tract pathology in a mouse model of genital infection.  Specifically, we are interested in delineating pathogen recognition by the host, signaling pathways that lead to the induction of innate immune cytokines in vitro and their downstream cellular effects in vivo.  We are specifically interested in understanding the contribution type I IFN, IL-1 activation, caspases and damage associated molecular patterns in pathogenesis. The identification of host molecules involved in amplification of the inflammatory response during infection, would serve as biomarkers and therapeutic targets to prevent reproductive sequelae in women infected with Chlamydia.

Pickles, Raymond J. email , , , publications

My laboratory, located in the Cystic Fibrosis/Pulmonary Research and Treatment Center in the Thurston-Bowles building at UNC, is interested in how respiratory viruses infect the airway epithelium of the conducting airways of the human lung.

Pylayeva-Gupta, Yuliya email , , , , publications

The goal of my research is to define molecular mechanisms of immune cell co-option by cancer cells, with the hope of identifying novel targets for immune cell reprogramming. Central to our approach is analysis immune cell subtypes in KRas-driven models of pancreatic cancer. We use cell and animals models to study signals important for pro-tumorigenic activity of immune cells, as well as define role of physiologically relevant oncogenic mutations in driving these signals and enabling immune escape.

Randell, Scott email , , , , , , , publications

Identification of airway epithelial stem cells; innate immunity in the airway; the pathophysiology of post-lung transplant ischemia reperfusion injury and bronchiolitis obliterans syndrome.

Samet, James M. email , publications

Our laboratory is focused on the cellular and molecular mechanisms that control  inflammatory and adaptive responses induced by inhalation of ambient air pollutants. Projects focus on early events that result in the disregulation of signaling processes that regulate gene expression, specifically oxidative effects that disrupt signaling quiescence in human lung cells. Approaches include live-cell imaging of human lung cells exposed in vitro and ex-vivo and characterization of oxidative protein modifications.

Sartor, R. Balfour email , , , , publications

Our long term goals are to better define mechanisms of chronic intestinal inflammation and to identify areas for therapeutic intervention. Research in our laboratories is in the following four general areas: 1) Induction and perpetuation of chronic intestinal and extraintestinal inflammation by resident intestinal bacteria and their cell wall polymers, 2) Mechanisms of genetically determined host susceptibility to bacterial product,. 3) Regulation of immunosuppressive molecules in intestinal epithelial cells and 4) Performing clinical trials of novel therapeutic agents in inflammatory bowel disease patients.

Serody, Jonathan email , , , publications

Our laboratory is involved in studies to determine the mechanisms and proteins involved in the migration of alloreactive and regulatory T cells to organs involved in graft-versus-host disease after stem cell transplantation using mouse models.

Sheikh, Shehzad Z email , , publications

We seek to understand how information is encoded and dynamically utilized in immune cells from healthy and disease prone intestines (The Inflammatory Bowel Diseases: Crohn’s disease and Ulcerative Colitis). Our lab is multi-disciplinary and combines high-throughput genomics with innate immunity and microbiology. We focus specifically on genes that regulate response to the bacteria that normally reside in our intestines. Many of these genes make products that regulate the immune system in the intestine. These products defend the intestine against the attack of foreign materials; such as bacteria that live in the intestine. We use genome-sequencing technology to precisely identify regions throughout the genome that are potential ‘on’ or ‘off’ switches for these genes. There is a fine balance between the genes that produce inflammatory substances that are necessary to kill bacteria and genes that produce anti-inflammatory substances that are important to prevent damage to the intestine. If this balance between inflammatory and anti-inflammatory substance production in the intestine is disrupted, IBD may result. Our lab focuses on understanding how these important controllers of inflammation are turned on and off in IBD. We also study how inflammatory and anti-inflammatory signals impact disease severity, progression and response to therapy in individuals with IBD. This information has the potential to increase our understanding of causes of IBD (personalized medicine) and to contribute to the development of new treatments.

Shiau, Celia email , , , , , , , publications

The Shiau Lab is integrating in vivo imaging, genetics, genome editing, functional genomics, bioinformatics, and cell biology to uncover and understand innate immune functions in development and disease. From single genes to individual cells to whole organism, we are using the vertebrate zebrafish model to reveal and connect mechanisms at multiple scales. Of particular interest are 1) the genetic regulation of macrophage activation to prevent inappropriate inflammatory and autoimmune conditions, and 2) how different tissue-resident macrophages impact vertebrate development and homeostasis particularly in the brain and gut, such as the role of microglia in brain development and animal behavior.

Su, Lishan email , , , , , , , publications

Major areas of research: 1) HIV-1 Virology, Immuno-Pathology and Immuno-Therapy, 2) HBV Virology, Immuno-Pathology and Immuno-Therapy, 3) Novel Immune Therapeutics Including Adjuvants and Vaccines, and 4) Humanized Mouse Models of Human Liver and Immune System.  My laboratory studies both virology and immunology of HIV-1 and HBV persistent infection.  We focus on defining viral factors that counteract host innate anti-viral immunity.  We have also developed humanized mouse models to study human immuno-pathology of chronic HIV-1 and HBV infection in vivo.  We investigate how human immune cells are dysregulated and contribute to diseases during HIV-1 and HBV persistent infection.  We are currently focused on the HIV-1/pDC/IFN-I axis that plays a critical role in HIV-1 persistence and AIDS, and on the HBV/Macrophage interaction in liver diseases.  In addition, we are developing novel immune modulatory therapeutics including antibodies, adjuvants and vaccines.

Su, Maureen A email , , , publications

Our lab is interested in understanding the genetics of autoimmunity using both mouse models and patient samples. Our work is highly translational and aims to have direct relevance to human disease. One of our approaches is to study rare Mendelian autoimmunity syndromes in order to determine the contributions of a particular gene to developing autoimmunity. We have focused on Autoimmune Polyendocrinopathy Syndrome Type 1 (APS1 or APECED), a rare condition due to mutations in the Autoimmune Regulator (Aire) gene. We are interested in how Aire promotes tolerance and have utilized both APS1 mouse models and patient samples to study this disease. We are also interested in understanding how dysregulation of the immune system results in Type 1 Diabetes Mellitus, an autoimmune disease in which beta cells in pancreatic islets are destroyed. We are primarily using patient samples to study how the balance of suppressor of effector arms of the immune system become dysregulated.

Thompson, Nancy email , , publications

The immune system is a network of interacting biological cells. The molecular events that lead to the activation and regulation of these cells often occur at the cell surface. However, little is known about the arrangement, motions and interactions of the participating cell-surface molecules. To examine these phenomena, we construct model cell membranes on planar supports from purified or synthesized molecules.  Recently developed techniques in laser-based fluorescence microscopy can then be employed to examine the behavior of select fluorescently labeled molecules at or near the supported planar membranes.  This research is significant not only in the basic understanding of the immune system, but also in other areas of cell-cell communication and cell membrane biophysics, in the physics of two-dimensional fluids, and in biotechnology.

Ting, Jenny email , , , , , , , , , , publications

Topics include gene discovery, genomics/proteomics, gene transcription, signal transduction, molecular immunology.  Disease relevant issues include infectious diseases, autoimmune and demyelinating disorders, cancer chemotherapy, gene linkage.

Tisch, Roland email , , , publications

Projects involve the study of cellular and molecular events involved in autoimmunity, and development and application of genetic vaccines to prevent and treat autoimmunity and cancer.

Vilen, Barbara email , , , , , publications

We are interested in understanding how autoreactive B cells become re-activated to secrete autoantibodies that lead to autoimmune disease.  Our research is focused on understanding how signal transduction through the B cell antigen receptor (BCR) and Toll Like Receptors (TLR) lead to secretion of autoantibodies in Systemic Lupus Erythematosus (SLE).

Wan, Yisong email , , , , publications

We are a molecular genetics laboratory studying immune functions by using mouse models. The focus of our research is to investigate the molecular mechanisms of immune responses under normal and pathological conditions. Our goal is to find therapies for various human immune disorders, such as autoimmunity (type 1 diabetes and multiple sclerosis), tumor and cancer, and inflammatory diseases (inflammatory bowel disease, asthma and arthritis).

Whitmire, Jason email , , publications

The Whitmire lab investigates how the adaptive immune system protects against virus infection.  The research is focused on understanding the mechanisms by which interferons, cytokines, and other accessory molecules regulate T cell numbers and functions following acute and chronic virus infections.  The goal is to identify and characterize the processes that differentiate memory T cells in vivo. The long-term objective is to develop strategies that improve vaccines against infectious diseases by manipulating these pathways.

Xiao, Xiao email , , , , publications

Xiao lab is interested in molecular medicine, specifically, gene delivery and therapy for various genetic and acquired diseases. The lab genetically engineers a non-pathogenic and defective DNA virus, named adeno-associate virus (AAV). The engineered AAV has all of its own genes gutted and replaced by our own genes of interests. As a result, the 22-nanometer AAV particles now serve as tiny FedEx/UPS trucks to deliver therapeutic genes to a variety of cells, tissues and even the whole body. Besides its superb efficiency, AAV also offers an excellent safety profile. For example, Xiao lab has developed AAV vectors to treat diseases like muscular dystrophies, heart failure, diabetes, arthritis, hepatitis and cancer, etc. A first of its kind gene therapy for Duchenne muscular dystrophy (DMD), a lethal childhood genetic disease, is in a phase I clinical trial.  In addition to gene delivery for therapeutic purposes, AAV can also be used as a powerful tool to study basic biology such as molecular genetics, signal transduction, apoptosis, mechanisms of pathogenesis and even the engineering of animal models. For example, AAV vectors can be used to deliver protein-encoding genes, antisense RNA, small interference RNA (siRNA) or microRNA to tissues like the muscle, heart, liver, pancreas, kidney, lung, brain and spinal cord, etc., to over-express, up-regulate or knockdown a gene or multiple genes for the purposes of dissecting particular molecular pathways, biological functions and immunology consequences and even creating disease models.