FACULTY

The Alam Lab focuses on mechanistic studies of asthma. We study molecular, signaling and cellular mechanisms of various endotypes of asthma.

Dr. Alper's laboratory is focused on understanding the regulation of the innate immune response, particularly as it relates to the basis for inflammatory disease.

My research focuses on antigen identification in optic neuritis, multiple sclerosis, neuromyelitis optica, and ocular inflammatory disorders.

Specializes in understanding how T cells develop and help fight infection.

Our research focuses on understanding the dynamic interface between the immune system, virus infection and tumorigenesis. These studies focus on how virus infection, and tumorigenesis are regulated at the single cell level and, in turn, how the immune system responds to these distinct challenges. This research is powered by genetic manipulation of the host and target cell, and strengthened by technical innovations in single-cell analysis using flow cytometry, mass cytometry, and multiplexed immunohistochemistry.

The Clark lab investigates bacterial-driven immune modulation in the respiratory tract. The upper respiratory tract is home to a diverse microbial community that includes both commensal and opportunistic bacterial pathogens. Research in the lab explores how exposure to these bacteria influences upper and lower respiratory tract inflammation and disease, with a focus on the innate immune response to acute infection.

The Colgan Lab studies mucosal inflammation with focus on intestinal inflammation in the context of inflammatory bowel disease and other GI diseases. Studies are aimed at understanding how epithelial and endothelial cells coordinate barrier function and inflammatory responses at mucosal surfaces. Our lab takes a multifaceted approach by investigating the relationships between gut microbiota, host immune system, genetic background, and environmental influences as it pertains to mucosal health and disease, with research emphasis on energy metabolism, host-microbe interactions, hypoxia-inducible factor, and innate immunity.

Research interests include: (1) CAR T and engineered T cell therapies of autoimmune diseases; (2) Mechanisms of T cell mediated metal hypersensitivities; (3) Mechanisms of T cell recognition of autoantigens in Type 1 diabetes and RA; and (4) Redox signaling and drug design in the immune diseases and infectious diseases.

The ultimate goal of research in my laboratory is to develop improved methods for measuring autoimmunity in type 1A diabetes, identify reagents that might have therapeutic utility for the prevention and/or treatment of this disease, and ultimately to translate this research to the clinic.

Our long-term goals are to develop novel approaches for treating immunorefractory cancers and to develop predictive models and diagnostics to identify compounds that sensitize tumors to T cell-based therapies.

Dr. Deane’s research is focused primarily on the preclinical period of rheumatoid arthritis (RA).

Exploring the conditions that foster somatic evolution and discovering cancer vulnerabilities.

My laboratory studies how dysregulation of pathogenic and protective T cells causes autoimmunity. We are specifically interested in the mechanisms underlying the autoimmune diseases Type 1 Diabetes and Systemic Sclerosis/Scleroderma. We focus on identifying the factors and pathways that enable autoreactive T cells to escape immune regulatory checkpoints and cause tissue damage, with the goal of using this knowledge for the development of innovative immunotherapies.

The overall interest of the Doran Lab is the study of host - pathogen interactions in the central nervous system and the female reproductive tract. Our studies focus on major human pathogens including Streptococcus agalactiae (also known as Group B Streptococcus, GBS), a leading cause of invasive disease in newborns and certain adult populations including pregnant women. We seek to elucidate the mechanisms by which GBS colonizes the vaginal tract during pregnancy and penetrates the blood-brain barrier in the newborn to cause meningitis, as well as characterize host response to infection and colonization.

Acute Lung Injury and Repair, Epithelial Injury, Fibrosis, Chronic respiratory infections, asthma.

The primary effort in my laboratory is to understand interactions between IgE and peanut allergens. In addition, we are working to understand cross-allergic reactivity between peanuts and tree nuts.

Our group focuses on epigenetic mechanisms regulating normal hematopoiesis and leukemia focusing on MLL-family histone methyltransferases.

Research in the Evans lab focuses on how airway mucins regulate respiratory health and disease. Two secreted mucins--MUC5AC and MUC5B--are the predominant macromolecular components of airway mucus. MUC5AC and MUC5B regulate host mucosal defense in health, but their excessive or aberrant expression is associated with transient infections and with a wide range of lung diseases such as asthma, cystic fibrosis, chronic obstructive pulmonary disease, pulmonary fibrosis, and lung cancer.

HLA gene editing in the treatment of autoimmunity.

We are interested in understanding how the immune system is dynamically regulated through cellular interactions and environmental cues. Using methods including in vivo microscopy and flow cytometry our goals are to elucidate mechanisms of immune activation and tolerance in autoimmunity, with the goal of developing therapeutic approaches for regulating the immune response.

Dr. Fry's research focuses on the preclinical and clinical development of chimeric antigen receptor (CAR) T cells for pediatric cancers.

My lab has investigated biological roles and molecular regulations of 1) IL-1, inflammasomes and autoinflammation in human melanoma and skin diseases; 2) IL-37 and immune tolerance; 3) Tumor heterogeneity and plasticity in melanoma and its therapeutic resistance; and 4) ALDH2 and melanocyte activation and melanoma.

Mechanisms of iNKT cell development and antigen recognition.

Axis Tunes PI3K Activity to Control Expression of Recombination Activating Genes in Early B Cell Development.

The primary interest of our lab is to understand how developmental genes are regulated during the multicellular developmental program of the bacterium Myxococcus xanthus, and the role of interactions between cells in regulating and coordinating this process.

My laboratory studies maternal effects on the immune system and development of allergic diseases, with a particular focus on asthma. Maternal effects are defined as influences of maternal environment, genotype or phenotype on the phenotype of the offspring. Maternal effects have been observed in a number of species, including mice and humans, for several environmental factors and in several tissues and systems of the offspring, including their immune system. Maternal effects may be beneficial, increasing offspring adaptation to changes in the environment and preventing a disease, and harmful, leading to a disease. List of maternally-influenced diseases includes asthma.

Our lab is interested in understanding the complexities of humoral immunity against rapidly evolving viruses. Our lab has three major interests: (1) Manipulating host factors to improve humoral immunity; (2) Zoonotic Influenza Viruses and Broadly Protective Humoral Immunity; and (3) Co-evolution of humoral immunity and influenza viruses.

T cell immunology, autoimmunity, type 1 diabetes. Our research is focused on the mechanisms and regulation of pathogenesis in the NOD mouse model of type 1 diabetes (T1D). We use cloned T cell lines and TCR transgenic mice to study the disease process. Our goals are to acquire better understanding of how CD4 T cells contribute to pathogenesis in T1D, investigate the beta cell autoantigens that activate autoreactive T cells, and develop new strategies for inducton of tolerance and prevention of disease.

Dr. Henson's primary areas of study are Cell biology, Inflammation, Apoptosis, Immunology and Phagocytosis. His Cell biology research incorporates themes from Receptor, Phosphatidylserine and Apoptotic cell clearance. His biological study spans a wide range of topics, including Tumor necrosis factor alpha, Immune system, Macrophage and Cytokine.

Research areas include: Airway Inflammation, Cystic Fibrosis (CF), Host Pathogen Interactions, and Pulmonary Disease.

Dr. Holers research group performs both basic and translational research. A longstanding interest has been to decipher the roles of complement receptors and membrane regulatory proteins in the immune response, with a special emphasis on autoimmune diseases.

Our lab addresses mechanistic and translational questions in human immunology using high-dimensional single-cell mass cytometry and ex-vivo cellular manipulation. Our goal is to enable a deeper understanding of normal immune function, and dysregulated immune processes in immunodeficiency, autoimmunity, and the overlap between the two.

The Huang laboratory studies transplantation immunology with a focus on developing clinically relevant protocols for the establishment of transplantation tolerance. Dr. Huang's research involves using basic immunologic approaches to develop clinically relevant strategies for regulating inflammation, overcoming transplant rejection and improving tumor immunotherapy.

My lab studies transcriptional and epigenetic regulation of genes that control immune effector cell development and regulate cytokine and chemokine gene expression. We investigate how super-enhancers and their associated transcription factors integrate signals triggered by various external stimuli, such as antigenic stimulation, infection, cytokine and metabolic products, to generate gene transcription outputs. We also determine the contribution of genetic variants to enhancer activity, gene expression and disease severity.

The long-term goals of our work is to understand how neuron-glial interactions modulate brain function and contribute to pathology in neurodegenerative disease. Towards this goal, we study the interactions of oligodendrocyte lineage cells with neurons in the adult cerebral cortex.

My laboratory is interested in understanding how a network of proteins called the cytoskeleton regulates the migration and cell-cell interactions of lymphocytes. In particular we focus on how the cytoskeleton generates the mechanical forces and shape changes required for lymphocyte migration and trafficking during homeostasis and disease.

His primary areas of study are Immunology, Acquired immunodeficiency syndrome, Internal medicine, Vaccination and Viral disease. His Immunology research is mostly focused on the topic Immune system. His work carried out in the field of Immune system brings together such families of science as Antibody and Antigen.

My research is focused on mechanisms of repair following acute and chronic lung injury. This includes studying how lung collectins influence alveolar macrophage phenotype, function, and fate in healthy lungs and during inflammation. I am also interested in the role that bone-marrow-derived stem cells (including endothelial progenitor cells) play in recovery from lung injury.

Dr. Karam’s laboratory is focused on basic and translational research related to head and neck and pancreatic cancer.

Our lab is interested in this curious boundary between the innate and adaptive immune systems and seeks to elucidate signals and pathways emanating from the various families of innate receptors most efficiently mediate the transition to the adaptive cellular immune response. In doing so, we seek to determine not only the basic rules of immunity, many of which remain elusive, but also to identify practical methods of intervention for the purposes of vaccine discovery, development and design.

The major focus of my research program is to elucidate pathways of innate immunity that can distinguish harmless microbes from pathogens, thereby enabling the host to mount responses that are commensurate with the threat.

The effects of advanced age and alcohol misuse on inflammatory responses after burn trauma or infection.

Dr. Kuhn’s research program focuses upon understanding mechanistic connections between the gut mucosa and joints in the development of spondyloarthritis and rheumatoid arthritis.

We study mechanisms of immune subversion and immune regulation during bacterial infections and other disease settings. We dissect strategies that microbes have evolved to thwart or manipulate immune responses and work to define host immune regulatory circuits that are manipulated by pathogens. Our studies focus on innate immune responses during mucosal and systemic infections. We are actively pursuing translation of information from our studies towards improved therapies for infectious, inflammatory, cancerous, and other diseases.

Our laboratory is interested in the basic biology of lymphocytes and application of knowledge about lymphocytes to human disease. Much of our work concentrates on T cells and their peculiar ability, via their aß T cell receptors (TCRs), to react with foreign antigens when these are bound as peptides to major histocompatibility complex proteins (MHC) of the host. We are interested in the structural reasons for this bias, the role of evolution in creating the bias, and the ability of T cells to distinguish between different alleles of MHC proteins, an ability which affects the health of the host and rejection of transplants.

Immune microenvironment regulation and immune evasion in brain tumors.

Emerging infections are a global public health threat. In the 21st century alone, we already have experienced devastating outbreaks of infectious disease, including diseases caused by mosquito-borne (e.g., chikungunya and Zika viruses) and respiratory RNA viruses (e.g., SARS-CoV-2). Our laboratory seeks to improve our knowledge of the molecular pathogenesis of these infections (i.e., what are the critical host-pathogen interactions that contribute to protection or pathology?) by addressing questions at the interface of immunology and virology/parasitology.

Her research strives to understand the mechanism of initiation of anti-beta cell autoimmunity. She focuses on the tri-molecular complex consisting of antigen, major histocompatibility complex (MHC), and T cell receptor (TCR) that could be a key component for the development of T1D. Her laboratory explores antigen specificity of autoreactive T cells having different functions (i.e. pathogenic vs regulatory T cells) that target pancreatic beta cells; the role of T cells expressing specific TCRs in the development of T1D using an animal model; the potential of TCR sequences to be used as T cell biomarkers to predict the development of type 1 diabetes as well as recurrence of hyperglycemia after clinical therapeutic trials; lastly, exploring the mechanism of transplantation failure in T1D patients.

The Norman lab researches immunogenetics, which is the study of polymorphic molecules that have critical roles during infection control, reproduction, cancer, and immune-mediated disease. We study the genetic and functional immune diversity of indigenous groups worldwide, including African hunter-gatherers, Australians and Pacific Islanders. We also study ancient humans, and perform comparative evolutionary analyses of multiple other species. The Lab focuses on the co-evolution of the HLA molecules that are expressed by healthy cells, and the KIR, which are Natural Killer (NK) cell receptors that interact with HLA to control immune cell activity.

Fungi are normal members of the human gut microbiome that are benign commensals in people. However, fungi can become pathogenic when the microbiome or immune system is perturbed. Candida species dominating the gut fungal community are notorious opportunistic pathogens capable of causing life-threatening disseminated infections. Candida species can also drive pathogenic inflammation in the gut and are associated with worsened inflammatory bowel disease in people. It is still largely a mystery as to how these fungi reside peacefully in the gut of most people. The goal of the Ost lab is to uncover the immune forces that constrain these fungi to a commensal state to prevent disease.

Our lab is interested in uncovering the molecular pathways that guide the development, selection and activation of autoreactive and non-autoreactive B cells and that, thus, lead to the generation of the naïve B cell repertoire.

Our lab studies host-pathogen interactions with the goal of defining host and bacterial pathways involved in bacterial persistence. Bacterial interactions with the host involve dynamic exchanges where heterogeneity from both sides can lead to many different outcomes. Persistence occurs when the pathogen evades the host immune response and the host is unable to clear the invading pathogen, resulting in stable bacterial colonization. Individuals with persistent infections often do not respond to long-term or repeated appropriate antibiotic treatment and, importantly, serve as reservoirs for the development of antibiotic resistance.

Interplay between inflammation and metabolism as a driver of leukemia development; targeting of pre-malignant and malignant blood-forming stem cells.

​The long-term goal of our research is to expand our understanding of the following five areas: 1) The cellular and molecular events that influence allergic disease susceptibility and initiation; 2) The mechanisms regulating immunity to parasites as a foundation for vaccine development; 3) The role and relationship between follicular T helper (Tfh), T-helper 2 (Th2), and follicular regulatory (Tfr) cells in the development/suppression of allergic and infectious disease, 4) The role of group 2 innate lymphoid cell (ILC2) subsets in mucosal barrier immunity, and 5) The mechanisms driving interferon-mediated autoinflammatory diseases.

Dr. Riches' career interests are focused on the intersection between lung immunity and fibrosis, and the role of macrophages and fibroblastic cells in these processes. Based on a combination of basic and translational approaches, his lab has made significant contributions to our understanding of the mechanisms underlying the development of pulmonary fibrosis, the mechanisms of macrophage functional programming, cytokine-induced signal transduction and the control of fibroblast and myofibroblast apoptosis. Dr. Riches' lab utilizes cutting edge approaches to model and analyze the development and resolution of pulmonary fibrosis in mice together with the study of comparable phenomena in lung tissues and primary cultured cells from patients with idiopathic pulmonary fibrosis and other fibrotic lung conditions.

The major areas of our research currently are: 1. Understanding how metabolism contributes to cancer chemoresistance and developing approaches to overcome chemoresistance; 2) Investigating MCJ as a target to enhance CD8 T cell mitochondrial metabolism and efficacy of CAR-T immunotherapy.

Our laboratory studies the interplay between the innate and adaptive immune response against retroviruses to conceptually advance vaccine and cure strategies against HIV/AIDS. We are specifically interested in “restriction factors” – host proteins that could directly inhibit retroviruses but we discovered also play critical roles in shaping adaptive immune responses. These factors could be regulated by Type I interferons, thus highlighting possibilities for clinical translation.

My research focuses on genetics and genomics of pulmonary fibrosis, gene discovery in innate immunity and epigenetics of environmental lung disease.

How T Cells recognize potentially harmful invaders.

Our lab specializes in translational research on multiple myeloma, a debilitating and incurable blood cancer. We are focused on developing new therapies, including both large-molecule immunotherapies and small-molecule pathway inhibitors. We are also developing approaches to personalize treatment through real-time monitoring of drug resistance development using ex vivo drug sensitivity testing.

Using an animal model for colon cancer, we are determining what substitutions in tumor antigen peptides improve antitumor immunity.

The Smith Lab focuses on how B-cells escape tolerance mechanisms to contribute to autoimmune disorders, such as type 1 diabetes.

The Tamburini lab focuses on understanding how immune cells interact and traffic through the lymphatic vasculature to facilitate an appropriate immune response. We are also interested in the trafficking of small molecules and antigens through the lymphatic vasculature and into draining lymph nodes during infection, vaccination or during chronic disease such as non-alcoholic steatohepatitis, alcohol related liver disease and primary schlerosing cholangitis.

We have a long-standing interest in investigating the mechanisms by which B lymphocytes develop and subsequently mount antibody responses to foreign antigens and pathogens. In the recent past we have particularly focused on understanding how the distinct B cell populations that exist in humans and mice act in concert to provide humoral immunity. To address these issues, we rely on molecular, genetic and biochemical in vitro and in vivo approaches that often rely on genetically-engineered mouse models. More recent work in our lab has revealed that a bioactive lipid, lysophosphatidic acid (LPA), is able to suppress signaling by both B and T lymphocyte antigen receptors and specifically upon engagement with the LPAR5 receptor.

His laboratory uses a variety of neurotropic viruses, including reoviruses, Enterovirus D-68, and Flaviviruses (West Nile, Japanese encephalitis and Zika) to study the pathogenesis of viral CNS infections. A particular interest has been in understanding the nature of specific cellular pathways (signaling, gene expression, apoptosis) that are activated during neurotropic viral infections and that lead to neuronal injury and death. The laboratory uses primary cell cultures, ex vivo slice cultures of brain and spinal cord, and murine models to study virus-cell interactions.

The van Dyk lab studies the interactions between virus and host in health and disease. Specifically, our work focuses on gammaherpesviruses.

The research in the Vázquez-Torres lab uses state-of-the-art biochemical, genetic and molecular biology approaches to understand the molecular mechanisms by which reactive species mediate resistance of macrophages against intracellular bacteria, as well as the adaptive strategies that boost antioxidant and antinitrosative defenses of pathogenic bacteria.

My research studies are aimed at developing cellular therapy to reduce leukemia recurrence by enhancing immune recovery and by more effectively treating sites of leukemia (with a newly developed method of bone marrow irradiation).

Pathogenic T cells, specifically in type 1 diabetes and multiple sclerosis.

1. Cellular immune response to HIV-1 and correlates of immune protection in early and chronic HIV-1 infection. 2. Development of novel prophylactic and therapeutic vaccines for HIV-1 infection 3. Immune reconstitution of HIV-1 infection 4. Interactions between HIV-1 and dendritic cells 5. Dendritic cell, T cell, and epithelial cell interactions in HIV-infected gut-associated lymphoid tissue (GALT) 6. HIV, aging, microbiome and mucosal immune function 7. Mechanisms of HIV-associated death in intestinal T cells 8. Role of Interferons in HIV pathogenesis.

We develop statistical machine learning for single-cell omics to study inflammatory disease for translational medicine.

RNA Polymerase II (Pol II) pausing is a unique transcription regulation mechanism in higher eukaryotes. We found that release of paused Pol II, phosphorylation of CTD-Pol II by CDK9, and cleavage of arginine methylated histone tails on + 1 nucleosome by JMJD5, are intrinsically coupled. We are trying to elucidate the underlying mechanism.

My research interest in cancer immunotherapy focuses on 1) identifying novel immune checkpoints, 2) characterizing pathways that limit intratumoral T cell infiltration.