Research/Research Labs

The Golenbock Lab spearheaded by Douglas Golenbock, MD, is interested in the innate immune response to infectious illnesses, especially Gram-negative infections related to the sepsis syndrome and malaria. Our focus has been on Toll-like receptors, inflammasomes and cytosolic DNA receptors that lead to interferonproduction. In addition to infectious diseases, we have a continued interest in Alzheimer’s Disease, and example of a sterile inflammatory disease that shares pathogenic mechanisms with infectious illness.

Research in the Caffrey Lab is focused on understanding the evolution and function of long non-coding RNAs (lncRNAs) in inflammation, the transcription and regulation of immune response genes and the evolution of host-pathogen interactions.

A major area of study in the Finberg Lab is examining the nature of the evolution of viruses in response to various selective pressures using a highly collaborative approach with systems biologists, bioinformaticians, virologists, and structural biologists. The Finberg laboratory has demonstrated the role of Toll-like receptors (TLRs) in the innate immune response to viruses and has identified the receptor for Coxsackie and Adenoviruses (CAR) as well as the receptor for many echoviruses (DAF). Our research has subsequently focused on pathogenesis and the development of the host immune response to respiratory viruses including influenza A virus (IAV) and respiratory syncytial virus (RSV).

The central goal of Fitzgerald Lab research is aimed at understanding the molecular mechanisms controlling the inflammatory response. We are interested in determining how the immune system discriminates between pathogens and host molecules to both protect the host from infection and avoid damaging inflammatory diseases. We employ multifaceted approaches including immunology, biochemistry, molecular biology and genetics to understand these mechanisms. Our long-term goals are to understand how dysregulation of innate immunity underlies the pathogenesis of infectious, inflammatory and autoimmune disease in humans.

The Fitzgerald Lab is part of the Program In Innate Immunity(PII) an interdisciplinary and interdepartmental group of investigators, who are focused on discovering the underlying mechanisms that drive immune defenses and inflammation, in both health and disease.

Dr. Laura Gibson's work as a clinician-scientist involves translational research focusing on the immunopathogenesis of cytomegalovirus (CMV) and other herpesvirus infection in populations at risk for severe disease, including neonates and solid organ transplant recipients.

Dr. Evelyn Kurt-Jones's lab studies the development of the innate immune response to DNA and RNA viruses, particularly in the lung and brain. Our focus is on TLRs and cytosolic innate immune signaling receptors and how these sensors promote the development of inflammation and adaptive immunity and influence disease outcome.

Fungal infections have emerged as major causes of morbidity and mortality, particularly in persons who are immunocompromised. The Levitz lab focuses on the mechanisms by which the immune system controls fungal pathogens and the strategies that fungi utilize to circumvent host defenses. Major ongoing projects in the laboratory include the development of a vaccine to protect at risk individuals against Cryptococcus neoformans and delineating the role of eosinophils in aspergillosis.

Research focuses on the development of vaccines and immunotherapeutic molecules to combat gonococcal infection as well as understanding the interactions of the immune system, specifically and complement, with the pathogenic Neisseria. 

The Lien lab is focused on understanding inflammation and host-pathogen interactions via Toll-like receptors (TLRs), NLR-inflammasomes, RIP kinases, inflammatory caspases and other signaling molecules. Model systems that we utilize include bacterial infections with Yersinia pestis (the causative agent of plague), Salmonella, other pathogens and also non-infectious inflammation. Furthermore, we are interested in vaccines and mechanisms for adjuvant action.

Research in the Pukkila-Worley Lab is focused on identifying innate immune pathways in the host and virulence-related signaling mechanisms in the pathogen that can be exploited to develop novel anti-infective small molecules. Towards this end, we are defining evolutionarily conserved means of innate immune activation using bacterial and fungal pathogenesis assays in the microscopic nematode Caenorhabditiselegans.

My group studies how bacteria (specifically, the bacteria that cause gonorrhea and meningitis) escape killing by the complement system. Knowledge of such immune evasion mechanisms are being translated to develop novel vaccines and therapies.

My research identifies unique bacterial determinants that serve as suitable vaccine candidates to protect against infection in humans. Usually these determinants activate complement (C) that combats invading bacteria and also facilitates and amplifies the development of adaptive immune responses. Under certain conditions, C-regulators are hijacked by microorganisms and down-regulate the activation and binding of active C components and divert organisms to non-professional phagocytes (epithelial cells) where they can gain sanctuary. In a separate line of inquiry, my laboratory also develops peptide mimics (immunologic counterparts [surrogates]) of suitable carbohydrate vaccine candidates to circumvent the disadvantages of carbohydrate-based vaccines. These simple peptides can then be used as vaccines to elicit protective immune responses.

My research focuses on the role of complement regulatory proteins in the pathogenesis of N. gonorrhoeae. The goal of my research is to develop novel therapies/vaccines against Neisseria gonorrhoeae which has become resistant to almost every conventional antibiotic.

The Silverman Lab is focused on illuminating the regulation of the innate immune and inflammatory responses in both insects and mammals. We are interested in how microbes are recognized by germline-encoded receptors and the molecular mechanisms involved in subsequent signal transduction pathways. In addition, we also examine how various environmental cues modulate innate immune responses. We rely heavily on the classic genetic model system of Drosophila melanogaster, the fruit fly, but also translate discoveries made in this model to more medically relevant systems, including vector mosquitoes  and mammals. Long-term, we aim to understand the molecular mechanisms that underly the innate immune response in the context of both health and pathophysiology.

The Lab is also a member of the Program In Innate Immunity (PII), an interdisciplinary and interdepartmental group of investigators who are focused on discovering the underlying mechanisms that drive immune defenses and inflammation, in both health and disease.

Currently, my research is focused on understanding the role of chitin and chitosan in organizing the cell wall of the pathogenic fungus, Cryptococcus neoformans. This has led to the pre-clinical development in a mouse model of vaccines that can resolve a cryptococcal lung infection.

Research in the Wang Lab involves studying innate immune responses to viruses including influenza, coxsackievirus, and herpes simplex virus. These innate immune responses are mediated by host pattern recognition receptors including Toll-like receptors and RNA helicases.