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Faculty

Katherine A. Fitzgerald

Katherine A. Fitzgerald

Dr. Fitzgerald is the Director of the Program in Innate Immunity. Research in the Fitzgerald lab is focused on understanding the molecular basis of host defense and the inflammatory process.  We are interested in cytosolic sensors that detect microbial or host nucleic acids, the role of innate immunity in malaria and the role of long non-coding RNAs (lincRNAs) in the regulation of inflammatory gene expression.  Our research uses immunology, molecular biology, biochemistry and genetics to understand these mechanisms. Our longer-term goals are to understand how dysregulation of sensing, signaling and gene regulation underlie the pathogenesis of infectious, inflammatory and autoimmune disease in humans. 

www.umassmed.edu/fitzgeraldlab


Douglas T. Golenbock

Douglas T. GolenbockThe Golenbock laboratory 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 interferon production.   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.


Daniel Caffrey

Daniel CaffreyResearch 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


Robert Finberg

Robert FinbergDr. Finberg’s research concerns cell surface receptors and the response of the host to everything from viruses to titanium particles. The laboratory uses both human cells and mouse models to measure responses to inflammatory stimuli.


John Harris

John HarrisIn the Harris lab we study vitiligo, an autoimmune disease where cytotoxic T cells migrate into the skin and destroy melanocytes, the pigment-producing cells. There is evidence that vitiligo begins with induced cellular stress within melanocytes, and that this stress activates innate inflammatory pathways. We are studying this process, and how innate inflammation translates into T cell-mediated autoimmunity.

www.umassmed.edu/vitiligo/


Evelyn Kurt-Jones

Evelyn Kurt-JonesMy 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.


Egil Lien

Egil LienThe 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.


Stuart Levitz

Stuart LevitzResearch in the Levitz laboratory is focused on the mechanisms by which the immune system controls specific fungal pathogens and the strategies that fungi utilize to circumvent host defenses. Particular areas of interest include how fungal glycosylation influences immune responses, inflammasome stimulation by chitosan, the mechanisms by which plasmacytoid dendritic cells mediate protection against Aspergillus fumigatus and the development of vaccines against Cryptococcus neoformans and other pathogens.


Read Pukkila-Worley

Read Pukkila-WorleyResearch 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 Caenorhabditis elegans. 

www.umassmed.edu/pukkila-worleylab/


Sanjay Ram

Associate Professor of Medicine

SanjayMy 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.


Peter Rice

Professor of Medicine

Peter RiceMy 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.


Ann Rothstein 

Ann rothsteinThe major focus of the Rothstein lab is to understand the role of innate immune sensors in the activation of autoreactive B cells and T cells in models of systemic autoimmunity, autoinflammation, and fibrosi. We use particular interested in responses to nucleic acid associated autoantigens and the interplay between cytosolic and endosomal sensors in the regulation of relevant effector populations. These studies depend on the analysis of mice gene targeted mice, as well as transgenics that express tissue specific “pseudo”-autoantigens, and novel bifunctional antibodies that deliver immune complexes to poyclonal B cell subsets and APC populations.


Neal Silverman

Neal SilvermanUsing Drosophila melanogaster as model system, the Silverman lab focuses on the molecular mechanisms and physiological systems that control innate immunity, especially NF-kB signaling.  Projects in the lab include identifying and characterizing innate immune sensing mechanisms involved in responding to bacterial or parasitic diseases, as well as elucidating the downstream signal transduction pathways.  Other projects in the lab focus on the control of the innate immune response by steroid hormones, and how this interaction changes with stress and/or age.  While the primary research approach uses Drosophila as model, we also translates our basic discoveries to other systems, like mosquitoes or mice, that are more immediately relevant to human diseases, often in collaboration with our colleagues in the Program for Innate Immunity.

Silverman Lab


Jennifer Wang

wang

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.