Marlene Bouvier, Associate Professor, Ph.D.

McGill University, Montreal, Canada, 1988

Our research activities are focused on investigating the central role that class I major histocompatibility complex (MHC) molecules play in the immune system.

More specifically, we are studying the molecular and mechanistic basis of the class I antigen presentation pathway. The cell-surface presentation of antigens by class I MHC molecules is the culmination of a complex process that takes place in the endoplasmic reticulum (ER) and involves the specialized proteins tapasin (TPN), calreticulin (CRT), ERp57, and the transported associated with antigen processing. In the last few years, we have characterized the biochemical and biophysical properties of TPN, CRT, and ERp57 to better understand their roles and modes of action within the class I assembly complex. More recently, we have elucidated the mechanistic basis by which TPN modulates the selection of antigens that bind onto class I molecules. Ultimately, this selection process critically influences cellular immune responses.

Given that the class I antigen presentation pathway is the first line of defense against viral infections and malignant transformations, it is not surprising that human viruses have evolved sophisticated strategies to downregulate the expression of class I molecules at the cell surface and suppress the recognition of viral antigens by cytotoxic T cells. Thus, another area of interest in our laboratory is to study the molecular basis of viral immune evasion mechanisms that operate by interfering with the class I antigen presentation pathway.

Ananda Chakrabarty, Distinguished University Professor, Ph.D.

University of Calcutta (India), 1965.

We have shown that bacteria such as Pseudomonas aeruginosa produce a protein called azurin that is secreted when the bacteria are exposed to cancer cells.  Azurin enters preferentially to cancer cells than normal cells.  Unlike anticancer drugs that target a specific step in the cancer progression pathway, azurin, and a modified form of azurin called Laz produced by Neisserial species, target multiple steps in the cancer progression pathways, thereby interfering in cancer growth both in vitro and in vivo.  Azurin and Laz are also highly effective in forming complexes with various surface proteins of the malarial parasite Plasmodium falciparum and the AIDS virus HIV-1, thereby significantly inhibiting their growth.  Thus a single protein such as azurin or Laz might have potential therapeutic application against such unrelated diseases as cancer, malaria or AIDS.The structural similarity of the proteins such as azurin with the immunoglobulin folds may explain the lack of immunogeicity of the bacterially derived azurin or Laz. A fragment of azurin, a peptide of 28 amino acids termed p28, has completed phase I clinical trial in Chicago in 15 stage IV cancer patients with refractory metastatic solid tumor. p28 showed no toxicity in such patients but significant beneficial effects including partial and complete regression of the tumors in several such patients. Currently p28 is undergoing clinical trials in several hospitals in pediatric brain tumor patients (

Zheng W. Chen, Professor and Director, M.D., Ph.D.

Peking Union Medical College (now Tsinghua University) 1988

Our lab is one of the front runners in the field of studying Ag-specific human/primate γδ T cells in infectious diseases. Our decades-long publications add to the literatures assessing these γδ T cells for Ag presentation/TCR recognition, innate-like features, memory-like characteristics, immune regulation, anti-microbial responses, homeostatic protection against lung damages, and anti-TB immunity. We provide 1st evidence implicating that dominant γδ T subset existing only in primates can protect against severe TB. Advanced studies of this γδ T subset are ongoing.

Our published studies also show that primate/human CD8+ CTL, CD4+ T helpers, Th1, and Th22 cells play roles in immunity against TB, demonstrating protective correlates of these T-cell subsets. We are currently studying how these anti-TB immunity components act in concert to mount protective responses against TB and immune mechanisms.

Our lab has demonstrated fundamental immunology and therapeutic effects for γδ T-cell-targeted intervention and Teff/Treg-based potential immnotherapeutics against TB and HIV-related TB. We now continue to develop and test immunotherapeutics against TB and MDR TB.

Our lab also has track records of additional NIH-funded research programs studying orthopoxvirus diseases, pneumonic plagues, malaria/HIV-related malaria and re-emerging poliovirus/poliomyelitis. Additional efforts are now focused on pathogenesis and translational science in the aspects of infection/immunity fundamentals, nano-biology/nano-medicine, mucosal vaccine candidate development, and re-purposing FDA-approved drugs for new therapeutics.   

Nancy Freitag , Professor, Ph.D.

University of California at Los Angeles, 1989.

Our lab is interested in deciphering how microbial pathogens cause disease and in defining host responses to bacterial infection.  We focus primarily on the food-borne intracellular bacterial pathogen Listeria monocytogenes as a model system for understanding how pathogenic intruders survive within infected host cells. L. monocytogenes is an environmental organism that can survive in the soil but which maintains the capacity to invade and replicate within mammalian cells.  The bacterium can cause life-threatening diseases in immunocompromised individuals, pregnant women, and neonates.  We are investigating bacterial factors that contribute to host infection as well those that direct bacteria to specific tissues.  We are additionally interested in how drugs that target the central nervous system can increase host susceptibility to bacterial infection, specifically anesthetics that are commonly used in surgery or within the ICU.  For these studies, we are including infection models of Staphylococcus aureus and Klebsiella pneumoniea.

Bin He, Associate Professor, Ph.D.

Purdue University, 1993.

Our laboratory studies viral infection and innate immunity.  We are interested in viral and host factors in cytokine expression, cell signaling, and pathogenesis.  We investigate viral mechanisms, with a focus on Toll-like receptor related innate immune pathways. By integrating molecular, genetic and systems biology approaches we aim to understand virus-host interactions pertinent to infectious as well as inflammatory diseases.

William Hendrickson, Associate Professor, Ph.D.

Tufts University, 1981.

I currently devote all my effort leading research core services for the university. I am Director of the Research Resources Center, which is part of the Office of the Vice Chancellor for Research. The RRC is comprised of 20 research cores and service units with 65 employees. I am also Director of Translational Technologies and Resources for the UIC Center for Clinical and Translational Sciences and Assistant Director of the UI Cancer Center. Most recently, I have devoted part of my effort in developing a $2.5M High Performance Computing Resource for UIC that is used for molecular modeling, engineering, imaging and genomics. My past interests were in basic molecular genetics of E. coli, specifically the transcription regulation mechanism of the L-arabinose operon. In addition my lab investigated the genome structure and pathogenesis of Burkholderia cepacia and related species, which are unusual bacteria possessing mutliple chromosomes. These organisms are important for bioremediation of toxic compounds in the environment and are also emerging pathogens, especially in cystic fibrosis patients.

Linda Kenney, Professor, Ph.D.

University of Pennsylvania 1987

Our laboratory is interested in signal transduction and the regulation of gene expression in prokaryotes. In particular, we are studying the two-component regulatory system EnvZ/OmpR that regulates the expression of outer membrane proteins as well as many other genes. OmpR is involved in regulating the expression of virulence genes in many pathogens. Our present work focuses on how OmpR activates genes required for systemic infection (located on Salmonella pathogenicity island 2) in Salmonella enterica.

Amy Kenter, Associate Professor, Ph.D.

Albert Einstein College of Medicine, 1982.

My research program is focused on immunoglobulin (Ig) isotype switching also called switch recombination (SR) which occurs at the Ig heavy chain locus and which is under developmental control. We have detected three DNA-binding proteins which bind to switch regions and which may be involved in the recombination process. We have also identified the presence of double strand breaks located in switch regions which are sequence specific, mitogen inducible and restricted to B lymphocytes.

My laboratory has recently developed a plasmid assay for SR. We are using this switch substrabe to map functional recombination motifs (FRMs) in switch DNA. This information is being used to identify isotype specific switching factors that our studies have revealed.

Howard Lipton, Professor, M.D.

University of Nebraska

Theiler's murine encephalomyelitis virus (TMEV) is an enteric virus and member of the Cardiovirus genus of the family Picornaviridae. Persistent infection of mice with low-neurovirulence TMEV provides a highly relevant experimental animal model for multiple sclerosis (MS). We are interested in elucidating the mechanisms that enable this ordinary lytic virus to cause persistent infection in macrophages recruited into the central nervous system (CNS) of mice. To this end, we are determining TMEV and host cell genes involved in apoptosis of murine macrophages and the role of TMEV carbohydrate co-receptors and protein entry receptor in infection and CNS persistence.

Alan Mclachlan, Professor, Ph.D.

University of Aberdeen (Scotland), 1980.

In my laboratory we study the regulation of HBV gene expression and its relationship to viral replication. In cell culture, we have identified and characterized many of the transcription factors that regulate HBV RNA synthesis and demonstrated a critical role of nuclear hormone receptors in viral tropism. Using HBV transgenic mice, the role of specific liver-enriched transcription factors in modulating HBV transcription and replication in vivo is currently under investigation. The importance of transcriptional regulation in the control of HBV replication in response to various physiological stimuli and metabolic states is also being characterized.

Bellur S. Prabhakar, Professor and Head, Ph.D.

The Johns Hopkins University, Baltimore, 1980

Dr. Prabhakar’ S laboratory is currently pursuing studies that are aimed at understanding the molecular pathogenesis of type-1 diabetes and thyroid autoimmune diseases, and apply lessons learnt from those studies to develop novel therapies to prevent development of and/or suppress ongoing disease. His studies on EAT have shown that GM-CSF can not only completely prevent the development of EAT but can suppress the ongoing disease. Similarly, mice treated with a bi-specific antibody with specificities for CTLA-4 and TSHR could prevent the development of EAT through the induction of antigen specific regulatory T cells that produce IL-10. Further studies are underway to fully delineate the underlying mechanism of GM-CSF action. These studies have been extended to understand the role of regulatory T cells in the NOD animal model of type1 diabetes (IDDM).

As part of his long-standing interest in type-1 diabetes, he recently cloned a novel human gene that is differentially expressed in human insulinomas and can encode four different splice variants. The most fascinating aspect of studies to date is that one of the splice variants (DENN-SV) is over expressed in tumors and cells expressing this variant are resistant to a number of cancer therapies. In contrast, another variant (IG20) is expressed at very low levels or not at all expressed in tumor tissues and renders cells highly susceptible to cancer treatments. Additionally, knockdown studies using SiRNAs have revealed that a 3rd isoform that is constitutively expressed, namely MADD is required for cancer cell survival. Efforts are underway to fully understand the physiological function of these proteins employing transgenic and knockout mice, and to develop novel therapies for cancer.

Lijun Rong, Associate Professor, Ph.D.

Purdue University, 1991.

Research in my laboratory focuses on the molecular mechanisms of enveloped viruses. We are using an integral approach of molecular, cellular, biochemical and structural techniques to identify and dissect essential features of the viral receptors and the viral envelope proteins required for viral/host membrane fusion and viral penetration. Currently we are working with viral glycoproteins of filoviruses, influenza viruses, hepatitis C virus (HCV), SARS-CoV, and Rous sarcoma viruses (RSV). These studies will provide important insights for molecular and cellular understandings of viral infections of these viruses. The information will be used to develop specific entry inhibitors to block viral infection and prevent viral diseases.

Deepak Shukla, Professor, Ph.D.

University of Illinois at Chicago, 1997

The major focus of our research is on understanding the early molecular events associated with viral invasion of human host cells. Using herpes simplex virus (HSV) as a model system we are trying to identify and characterize the viral and cellular components including intra- and inter-cellular signaling pathways that facilitate HSV entry into host cells and spread to uninfected neighboring cells. We are using a multifaceted approach involving genetics, molecular biology, biochemistry and cell biology to achieve our goals. We are also interested in testing our findings in primary human cells and in vivo using a mouse model of the disease. In addition, a significant portion of our research interest is dedicated to developing novel anti-viral agents both as tools for understating the viral invasion mechanisms and future candidates for drug development.

David Ucker, Professor, Ph.D.

University of California, San Francisco, 1981.

Cell death serves a critical physiological process in organismal development, in the shaping of functional cellular networks, and in homeostasis. Our work focuses on the cell autonomous mechanism by which cells effect their own orderly demise, as well as the process by which dead cells assure their non-inflammatory clearance by phagocytic cells. We have examined death-associated events in different apoptotic death responses in a variety of cell types, and we have exploited death-inhibitory gene products to map the order of action of the associated activities.
This work has led to the identification of a thematically conserved cell death pathway. We have defined operationally a point of death commitment by distinguishing necessary and non-lethal [modulatory] steps from those [effector] steps that cannot be dissociated from actual death. Remarkably, we find that the requisite activities of caspases (the family of death-associated cysteine proteases), functioning in a cascade punctuated by Bcl-2, map primarily to the modulatory phase of the process, while cyclin dependent kinase (Cdk) activity, normally associated with cell division and activated in a caspase-dependent manner during cell death, is a critical effector phase constituent. Current efforts seek to identify the critical targets of lethal Cdk action. Our studies of clearance have revealed that the recognition of apoptotic cells is coupled directly to anti-inflammatory responsiveness on the level of transcription, and reflects a profound innate immunity that discriminates live from dead cells without regard to self. We are identifying specific determinants for apoptotic recognition and inflammatory modulation, and delineating the processes within the dying cell that lead to the expression of those determinants. A more complete understanding of the regulation, mechanism, and outcome of the physiological cell death process will offer insights to normal cell and tissue development, and provide new views of aging and treatments for pathological conditions including autoimmune diseases, chronic inflammation, and cancers.

Susan Uprichard, Assistant Professor, Ph.D.

Harvard University, Cambridge MA 1996

The objective of our research is to facilitate the development of effective antiviral therapies and vaccines against Hepatitis C Virus. Although HCV infects more than 2% of the world population and represents a significant public health burden, research efforts to understand HCV infection have been hindered by the lack of experimental systems. For this reason, one initial and continuing focus of the laboratory is the establishment, characterization, and optimization of the experimental in vitro cell culture and in vivo mouse models needed to dissect the HCV life cycle, understand molecular mechanisms of HCV-associated liver disease, and identify the viral-host interactions that determine the outcome of infection. Additionally, projects utilizing our newly established infectious HCV cell culture system include the study of the viral-host interactions that regulate the intracellular trafficking of the virus (e.g. entry, uncoating, assembly, and egress), development of a high throughput screening platform to identify potential HCV inhibitors, genomic screens to identify host cell factors that regulate viral infection, and investigation of RNAi therapeutics for the treatment of chronic HCV infection.

Karl Volz, Associate Professor, Ph.D.

University of California, San Diego, 1981.

In all processes of living cells, form and function are defined by molecular structure and intermolecular recognition. These principles of life are accessible through X-ray crystallography, the only technique for visualizing three-dimensional structures of biological macromolecules at atomic resolution. Using crystallographic approaches, we have analyzed the structural determinants of proteins that regulate "two-component" signal processing systems in bacteria.

William E. Walden, Professor Ph.D.

Washington University, 1983


The research focus of my laboratory is on the post-transcriptional regulation of genes of iron transport, storage and utilization, and on the regulation of iron homeostasis in eukaryotes. I am also interested in the mechanisms of translational regulation, specifically translational control via sequence specific RNA binding proteins. A main focus of our work is on the Iron Regulatory Proteins of animal cells.