Member Details

Lena Al-Harthi, MD
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312/563-3220

Pedro Avila, MD
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312/503-0075

Edward Barker, PhD
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312/942-3136

Linda Baum, PhD
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312/942-2881

Bruce Bochner, MD
410/550-2101

Kenneth Boyer, MD
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312/942-8928

Melissa Brown, PhD
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312/503-1013

Paul Bryce, PhD
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312/695-4000

Kent W. Christopherson II, PhD
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312/563-2522


Joan_Cook-Mills
Joan Cook-Mills, PhD
Associate Professor, Allergy-Immunology Division,
Northwestern University Feinberg School of Medicine
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312/503-0906

Current Research
Endothelial Cell Function during Allergic Disease: Leukocyte migration from the blood into tissues is vital for immune surveillance and inflammation. Specificity for the site of leukocyte migration is determined by the combination of adhesion molecules, cytokines and chemokines in the microenvironment. Research has focused on the function of the endothelial cell adhesion molecule VCAM-1. VCAM-1 is expressed on endothelial cells during atherosclerosis, allograft rejection, infection, and asthmatic responses. Dr. Cook-Mills' team has reported that VCAM-1 activates endothelial cell intracellular signal transduction pathways which result in endothelial cell shape changes and allow leukocyte passage. Currently, there are two main research directions: 1) Determine mechanisms for VCAM-1-stimulated activation of endothelial cell NADPH oxidase, including studies of the structure/function of the cytoplasmic tail of VCAM-1. They are also examining signals downstream of NADPH oxidase that regulate cell function. 2) Determine whether VCAM-1 signals function in vivo by utilizing knockout and transgenic mouse models to examine VCAM-1-dependent infiltration of eosinophils in experimental asthma. Information about the mechanisms that control leukocyte infiltration will provide a basis towards proposing interventions in VCAM-1-mediated processes in disease.

Corey
Seth J. Corey, MD, MPH
Associate Professor, Division of Pediatrics,
MD Anderson Cancer Center, University of Texas
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713/792-9511

Current Research
Dr. Corey's lab studies kinase signaling in hematopoiesis. Using G-CSF Receptor as a model system in mouse and man for cytokine receptor signaling, we are investigating the roles of the Src kinase Lyn and PI 3'kinase. Aberrant G-CSF Receptor function occurs in some forms of neutropenia and leukemia. Using Lyn as bait in a yeast two hybrid screen, we discovered a new cytoskeletal protein CIP4 (Cdc42 interacting protein 4). Having generated the CIP4 knockout mouse, they are now characterizing its defects in intracellular trafficking and endocytosis. Because cell signaling consists not only of pathways but also of circuits and networks, they are applying the principles of systems biology to granulopoiesis and cytoskeleal reorganization.

Syamal K. Datta, MD
Professor of Medicine,
Professor of Microbiology-Immunology,
Northwestern University Feinberg School of Medicine
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312/503-8197

Current Research
Dr. Datta's major research interests include: mechanisms of autoimmunity to nuclear antigens in lupus; molecular pathways of activation-induced cell death; develop antigen-specific tolerance therapy to restore immunoregulation and maintain lupus patients in remission. Dr. Datta's team has established that in systemic lupus (SLE), the immune system responds abnormally to nucleosomes, the major products of apoptosis (J Exp Med. 177:1367, 1993). Their main research programs involve studies on the origins of autoimmune response to nucleosomes, and signaling defects in autoimmune T and B cells that lead to abnormal co-stimulation and apoptosis-resistance. Work is progressing in parallel in lupus patients and mouse models of lupus we developed (Nature 263:412, 1976). They have identified nucleosomal peptide epitopes critical for cognate interactions between the autoimmune T helper (Th) cells and anti-DNA B cells in murine and human lupus (J Exp Med 183:2459, 1996). Tolerance therapy with the peptides is effective for blocking or treating established lupus autoimmunity by generating tolerogenic dendritic cells and potent subsets of regulatory T cells that cause "tolerance spreading."

Isabelle De Plaen, MD
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312/755-6379

Leon Epstein, MD
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773/880-4352

Ramsay Fuleihan, MD
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773/880-3710

Anita T. Gewurz, MD
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312/942-4912

Leslie C. Grammer, MD
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312/695-4000

Nadim Hallab, PhD
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312/942-2808

Karpus
William J. Karpus, PhD
Marie A. Fleming Research Professor,
Professor of Pathology,
Professor of Microbiology-Immunology,
Director, Integrated Graduate Program,
Northwestern University Feinberg School of Medicine
Associate Director of Flow Cytometry, Northwestern Memorial Hospital
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312/503-1005

Current Research
The central theme of Dr. Karpus’ research program is the role of chemokines and chemokine receptors in the regulation of autoimmune disease, chronic viral diseases, mucosal immunity and trafficking of B lymphoma cells. Specifically, chemokine regulation of dendritic cell and macrophage trafficking and chemokine regulation of T cell effector function in experimental autoimmune encephalomyelitis (EAE); chemokine receptor regulation of chronic disease progression in Theiler’s murine encephalomyelitis virus (TMEV)-induced demyelinating disease; and chemokine expression in lymphoid and non-lymphoid tissue and regulation of the migration of lymphoma cells expressing specific chemokine receptors to those particular tissues.

Jennifer Kim, MD
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773/327-3710

Marisa Klein-Gitelman, MD
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773/880-4360

Katherine Knight, PhD
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708/216-8723

Rajesh Kumar, MD
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773/327-3710

Alan Landay, PhD
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312/942-2849

Thomas Lint, PhD
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312/942-5986

Peter Lio, MD
Assistant Professor of Dermatology,
Northwestern University Feinberg School of Medicine
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312/695-0435

Current Research
Dr. Lio has an interest in atopic dermatitis/eczema and autoimmunity in the skin. He is currently working to establish an Eczema Care and Education Center as part of the Department of Dermatology that will focus on treatment of eczema from infancy to adulthood using a multi-specialty approach, including alternative and complementary medicines and techniques.

Judith Luborsky, PhD
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312/942-6602

Michael Miller, MD
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773/880-4360


SDM-2005
Stephen D. Miller, MD
Professor and Director, Immunobiology Center,
Department of Microbiology-Immunology,
Northwestern University Feinberg School of Medicine
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312/503-7674

Current Research
The Miller Lab studies the cellular and molecular mechanisms of multiple aspects of the immunopathogenesis and specific immunoregulation of T cell-mediated autoimmune responses. The laboratory mainly employs two mouse models of multiple sclerosis (MS) - Theiler's virus-induced demyelinating disease (a virus-induced model of MS) and Relapsing Experimental Autoimmune Encephalomyelitis (R-EAE), an autoimmune model of MS. Using the EAE model, the laboratory is examining the role of epitope spreading (the process whereby self tissue destruction results in activation and recruitment of autoreactive T cells and B cells specific for self antigens distinct from that which initiated disease). In addition, a major emphasis of the laboratory is to determine the efficacy and cellular and molecular mechanisms of controlling ongoing autoimmune diseases by antigen-specific immunoregulatory strategies including peptide-specific tolerance, regulatory T cells, and antagonism of T cell costimulatory molecule pathways (eg, B7/CD28 and CD40/CD40L) which are applicable to the treatment of both autoimmune diseases and cancer. Using the Theiler’s virus-induced demyelinating disease model, they are studying the roles of epitope spreading and molecular mimicry (the process whereby immune responses to viral epitopes cross-react with self tissue determinants) in both the initiation and chronic progression of virus-induced autoimmune pathology. The lab is also studying both the role of innate and adaptive immune regulatory functions controlling virus replication, clearance and persistence in CNS tissue. Lastly, they employ the NOD model of type 1 diabetes to study the efficacy of tolerance-based immunotherapy for regulating the diabetogenic autoimmune response and for regulating rejection of islet allografts.

Giselle S. Mosmain, MD
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312/942-4916

James Moy, MD
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312/942-6176


MullerWilliamJ
William J. Muller, MD, PhD
Assistant Professor of Pediatrics,
Northwestern University Feinberg School of Medicine
Attending Physician, Division of Pediatric Infectious Diseases,
Children’s Memorial Hospital
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773/880-4187

Assistant Professor of Pediatrics,Northwestern University Feinberg School of MedicineAttending Physician, Division of Pediatric Infectious Diseases,Children’s Memorial Hospital 773/880-4187

Current Research
Dr. Muller’s research goal is the development of vaccine candidates for herpes simplex virus (HSV), and understanding the immune responses necessary to create effective HSV vaccines. His first research area involves altering the receptor-binding characteristics of the virus to create a recombinant HSV which cannot infect neurons, and therefore will not establish latency. This recombinant virus would be a potential vaccine candidate. Related projects test immunity generated after infection with mutant HSV unable to bind to its natural cell surface receptors, at least one of which is involved in immune signaling. Preliminary data suggests that abrogating binding to this natural HSV receptor alters early inflammatory cytokines and possibly modifies cellular immune responses. A second research area investigates lymphocyte trafficking in response to mucosal vs. systemic delivery of virus, and how expression of specific lymphocyte surface molecules may be altered based on route of immunization.

Timothy Niewold, MD
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773/702-1234

Hans Ochs, MD, PhD
206/987-7450

Maurice RG O'Gorman, PhD, MBA
Co-director, Chicago City-wide FOCIS Center of Excellence
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773/880-4361


Lauren M. Pachman, MD
Lauren M. Pachman, MD

Co-director, Chicago City-wide FOCIS Center of Excellence
Director, Cure JM Program of Excellence in Juvenile Myositis Research
Professor of Pediatrics, Northwestern University Feinberg School of Medicine
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773/755-6381

Current Research
Immunobiology and Immunotherapy of Juvenile Dermatomyositis: The current focus of this research team is the pathophysiology of Juvenile Dermatomyositis (JDM) the most common of the pediatric inflammatory myopathies, in which small blood vessels are attacked by the immune system. Little is known about the environmental and genetic risk factors associated with the development of the classic clinical symptoms of rash and often profound weakness. There is less information about the physical outcome of this chronic and sometimes fatal illness—including one of the most troubling complications, pathological calcifications—which are a major contributor to morbidity. A specific goal of this laboratory is to identify the most effective route/dose of the most commonly used drug for JDM, prednisone, and to develop targeted, effective interventions.

Amy Paller, MD
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312/695-3721

C. Lucy Park, MD
Head, Division of Allergy-Immunology & Pulmonology,
Department of Pediatrics, University of Illinois at Chicago
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312/996-6714

Current Research
Dr. Park's research interests include pathogenesis of autoimmunity associated with immunodeficiency, diagnostic evaluation and management of immunodeficiency disorders, and physician education on immunodeficiency disorders. Her expertise is primary and secondary immunodeficiency disorders.

Janet Plate, PhD
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312/942-3450

Jacqueline Pongracic, MD
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773/327-3734

Richard M Pope, MD
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312/503-8003

Bellur S. Prabhakar, MD
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312/996-4945

Adrienne Prestridge, MD
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773/880-8150

RRG_picture
Rosalind Ramsey-Goldman, MD, DrPH
Solovy-Arthritis Research Society Research Professor,
Professor of Medicine,
Division of Rheumatology,
Associate Program Director, Clinical Research Unit,
Northwestern University Feinberg School of Medicine
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312/503-8003

Current Research
Dr. Ramsey-Goldman is the Principal Investigator for the Patient-Oriented Clinical Research Program in Systemic Lupus Erythematosus (SLE), (funded by NIH grants and foundation support) investigating SLE prevention, and its osteoporosis, cancer, and CVD-related complications. Through national and international collaborations, she is also studying genetic risk factors for disease susceptibility and severity in SLE. She is also active in designing, monitoring, and performing clinical trials testing innovative therapies for patients with SLE.

Anne H. Rowley, MD
Professor of Pediatrics,
Professor of Microbiology-Immunology,
Northwestern University Feinberg School of Medicine
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773/880-4187

Current Research
Etiology and Pathogenesis of Kawasaki Disease (KD): KD is an acute multisystem inflammatory illness of childhood that particularly affects the coronary arteries, and can lead to myocardial infarction and sudden death. It is the leading cause of acquired heart disease in children in developed nations. Dr. Rowley's laboratory studies the etiology, pathogenesis and immunology in acute KD, in particular our discovery that cytoplasmic inclusion bodies targeted by the acute KD IgA response are present in acute KD ciliated bronchial epithelium. The inclusion bodies are most consistent with aggregates of viral protein and associated nucleic acid; identification of these proteins and nucleic acids is ongoing in the lab.

Robert P. Schleimer, PhD
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312/695-4000

Girish D. Sharma, MD, MBBS
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312/563-2270

Stanford T. Shulman, MD
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773/880-4262

Gregory Spear, PhD
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312/942-2083

Rachel Story,MD
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773/327-3710

Xiao-Di Tan, MD
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773/755-6380

Allan R. Tenorio, MD
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312/942-5865

Larry L. Thomas, PhD
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312/942-3518

Mary C. Tobin, MD
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312/942-6296

William Tse, MD, PhD
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773/755-6382

George Tsokos, MD
617/667-0751

John Varga, MD
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312/503-8003

Barry Wershil, MD
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773/880-8368

Cornelia Weyand, MD, PhD
404/727-7310

Susan Winandy, PhD
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312/503-3075

Ram Yogev, MD
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773/880-2713

Byung H. Yu, MD
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312/942-6296

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