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Immunology and Microbiology Program

Immunology, virology, and bacterial pathogenesis are active interdisciplinary biomedical fields with studies ranging from molecular mechanisms to clinical trials. The Immunology and Microbiology Program (IMP) is administered by an interdepartmental group that includes faculty with diverse research interests, including the molecular and cellular basis of immune responsiveness, molecular mechanisms of viral replication, host-pathogen interactions, and the control of viral, bacterial and parasitic infections.


All Basic Biomedical Science students must complete the core curriculum as well as electives required by their program. Students in the Immunology and Microbiology program must take 3 elective courses. Students should take Infection and Immune Response in the first year, and, in the second year, at least one advanced level course offered by the Immunology and Microbiology program. Equivalent elective courses can be substituted with permission. All students, except for those in the final stages of their dissertation research, are required to take Graduate Student Seminar each fall semester, and Immunobiology and Microbiology Seminar and Discussion, or an equivalent guest scientist seminar program, for two semesters.

View PhD Program Schedule  |  View Courses



Ann Moormann, PhD, MPH
email Dr. Moormann

Neal Silverman, PhD
email Dr. Silverman  |  Silverman Lab

Trudy Morrison, PhD
email Dr. Morrison  |  Morrison Lab

Beth McCormick, PhD
email Dr. McCormick  |  McCormick Lab


Research areas of our faculty include:

  • Viral and bacterial immunology and pathogenesis
  • Molecular virology
  • Diabetes and transplantation immunology
  • Molecular and cellular immunology
  • Vaccine development
  • Host response against bacterial and viral pathogens
  • Innate immune mechanisms
  • Systems biology of host-pathogen interactions
  • Microbiome sciences

View the affiliated faculty listing for the Immunology and Microbiology Program.



IMP hosts an annual retreat featuring our faculty and students presenting their more recent research, as well as an invited keynote speaker.  The keynote speakers usually attend for the duration of the retreat and add a great perspective with their Q&A during talks and poster presentations. Recent keynote speakers have included Ramnik Xavier (MGH), Greg Barton (UC Berkeley) and Neal Alto (UTSW). In addition to the retreat, IMP organizes a robust, semester-long seminar program where outside experts in the field visit campus for a day, present their current research and interact with students and faculty.  In addition, IMP organizes several social and informational sessions each fall to welcome new students. 

Many training-grant eligible IMP students are supported by T32 for one or more years. Training grants include:


Getting Results…
  • MD/PhD candidate seeks to improve health by understanding host-pathogen interactions
    Education News, Media

    MD/PhD candidate seeks to improve health by understanding host-pathogen interactions

    MD/PhD candidate Nick Peterson is studying host-pathogen interactions in the Division of Infectious Diseases and Immunology and is co-chair of the MD/PhD Curriculum Committee.

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  • Immunology and microbiology PhD candidate aims to use her voice in science policy career
    Education News, Media

    Immunology and microbiology PhD candidate aims to use her voice in science policy career

    PhD candidate Sarah Cleveland’s mission is to ensure that diverse voices are represented and heard. Cleveland, who studies mechanisms of T cell tolerance, wants to pursue a career in science policy after earning her degree.

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  • Nick Peterson and Samantha Tse named Ruth L. Kirschstein National Research Service Award recipients
    Research News

    Nick Peterson and Samantha Tse named Ruth L. Kirschstein National Research Service Award recipients

    Two MD/PhD students in the lab of Read Pukkila-Worley, MD, have each received Ruth L. Kirschstein National Research Service Awards from the National Institute of Health.

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  • Samantha Tse, Pukkila-Worley Lab, Funding provided by National Institutes of Health

    Detection of intestinal pathogens through host surveillance of bacterial toxins

    Although commensal and pathogenic bacteria can be recognized by host pattern recognition receptors, intestinal epithelial cells target protective inflammatory responses towards pathogenic organisms through mechanisms that are incompletely understood. Additional mechanisms of pathogen sensing must exist that allow intestinal cells to target inflammatory defenses towards bona fide pathogens during an infection, and not harmless commensal bacteria. Pathogenic bacteria can express virulence determinants. Phenazine toxins are a family of redox active virulence determinants that are produced by a variety of human pathogens, including P. aeruginosa. P. aeruginosa can colonize the intestines of immunocompromised patients and cause fulminant septicemia and subsequent death. The mechanism by which intestinal epithelial cells detect P. aeruginosa, and whether this involves the surveillance of phenazine toxins, is not known. Nuclear hormone receptors (NHR) are transcription factors that program adaptive host responses following recognition of specific exogenous or endogenous ligands. In particular, HNF4⍺ is an NHR expressed in the intestine. In the model organism C. elegans, the HNF4⍺ homolog NHR-86 is required for the transcriptional activation of innate immune effector genes that protect against P. aeruginosa infection. The central hypothesis of this proposal is that intestinal epithelial cells detect infection through the surveillance of pathogen-derived phenazine toxins by NHR-86/ HNF4⍺, which directly activates protective anti-pathogen defenses in the intestinal epithelium. The following key preliminary findings support this central hypothesis: i) P. aeruginosa mutants that cannot make phenazine toxins do not activate C. elegans innate immune defenses; ii) synthetic phenazine toxins can activate immune genes; and iii) induction of immune genes by phenazine toxins is dependent on the expression of NHR-86/ HNF4⍺. In this proposal, Aim 1 will characterize the C. elegans immune response towards bacterial phenazine toxins, and Aim 2 will define the role of intestinal NHR-86/HNF4⍺ in detecting P. aeruginosa infection in C. elegans. The research proposed here will define a new concept of immune activation in intestinal epithelial cells and will also attribute a novel role for NHRs in pathogen sensing in the intestine. Insights from these findings may identify unexplored approaches for the development of anti-inflammatory and anti-infective therapies.

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    Mechanism of epigenetic inheritance in a mouse model of acute paternal stress

    Epigenetic inheritance is a process by which parental exposure to environmental factors influences offspring phenotype. This field of investigation has wide-ranging implications for human health. Epidemiologic studies have shown that exposure of parents or grandparents to starvation, trauma, cigarette smoke, or other stressors alters offspring susceptibility to cardiovascular disease, obesity, lung disease, or other conditions. Research with animal models has mirrored these findings and offers tools for disentangling the underlying mechanisms of epigenetic information transfer from parent to offspring. Such research has been greatly enabled by recent technological advances, including next generation sequencing and fundamental discoveries like microRNA biology. In vitro fertilization experiments demonstrate that sperm carry sufficient information to propagate epigenetic phenotypes across generations, and research with these paternal epigenetic inheritance models has identified sperm-associated small non-coding RNAs (sncRNA) as carriers of information from father to offspring. I have established an epigenetic inheritance model in which paternal influenza infection, with virus elimination and disease recovery prior to mating, results in an adaptive attenuation of disease severity (significantly decreased weight loss) in response to influenza infection in offspring, as well as a maladaptive altered glucose metabolism. While these phenotypes are robust, the underlying mechanism of information transfer to offspring remains to be determined. In preliminary experiments to address the mechanism I have found that influenza infection alters sperm-associated sncRNA. This proposal addresses the hypothesis that influenza virus-induced changes in sperm-associated sncRNA populations alter embryo development resulting in offspring metabolic and immune phenotypes. Aim 1 elucidates the underlying epigenetic inheritance mechanism through kinetic analysis of sperm sncRNA and early embryo development. Aim 2 determines the specificity of the offspring epigenetic inheritance phenotype to the paternal stressor both directly by challenging with a non-cross reactive strain of influenza virus, and indirectly by further metabolic phenotyping to determine if paternal influenza infection alters glucose homeostasis and liver gene expression in the offspring in ways similar to other paternal stressors. This research will provide valuable insight into the mechanism underlying epigenetic inheritance, and do so within the context of a novel epigenetic inheritance model with direct relevance to human health.

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  • Peterson.jpg

    Pathogen sensing by nuclear hormone receptors in C. elegans intestinal epithelial cells

    The mechanisms of pathogen sensing and immune effector induction in intestinal epithelial cells are not completely understood. Disruption in the mechanisms of pathogen sensing and immune homeostasis in intestinal epithelial cells can lead to dysbiosis and inflammation, as well as susceptibility to bacterial infection. Key insights into intestinal epithelial cell immunity and host-pathogen interactions have been made using the nematode C. elegans. Nematodes mount innate immune defenses against bacterial infection via conserved immune pathways, but the mechanisms of pathogen detection are unknown in this organism. In nematodes, the family of nuclear hormone receptors (NHRs) has dramatically expanded compared to other metazoans. NHRs are ligand-gated transcription factors that sense endogenous and exogenous signals to induce adaptive transcriptional responses. The C. elegans genome encodes 274 NHRs, of which 260 are homologs of human HNF4α. HNF4α is a key NHR involved in inflammatory bowel disease, though the mechanism through which HNF4α mediates inflammatory bowel disease in humans is unknown. The central hypothesis of this proposal is that C. elegans HNF4α homologs are an ancient family of pathogen sensors whose evolutionary expansion in C. elegans was driven by their function in detecting diverse pathogens. The following key findings support this hypothesis: (i) The nuclear hormone receptor, NHR-86/HNF4α, senses the cellular environment and activates C. elegans intestinal immune defenses; (ii) NHR-86/HNF4α is required for pathogen resistance and immune response towards the gram positive human pathogen E. faecalis; and (iii) A different C. elegans HNF4α homolog is required for pathogen defense and immune effector regulation against the gram negative pathogen P. aeruginosa. In this proposal, Aim 1 will define the role of C. elegans NHR-86/HNF4α in pathogen detection and immune effector induction during E. faecalis infection using a combination of transcriptomics, ChIP- sequencing, tissue-specific rescue and genetic epistasis. Aim 2 will characterize the function of a separate C. elegans HNF4α homolog in pathogen sensing during P. aeruginosa infection. The approach includes: transcriptomics, global NHR binding site identification, tissue specific rescue, and P. aeruginosa genetics. Collectively, these studies will characterize a fundamentally new paradigm of immune activation, which will solve a major conundrum of how pathogens are sensed in C. elegans. These findings will also establish NHRs as evolutionarily ancient pathogen sensors. Ultimately, the expectation is that detailed dissection of this mechanism will shed light on the role of HNF4α in mammalian pathogen sensing and inflammatory bowel disease.

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    Investigating the role of B cells in pulmonary fibrosis resulting from STING gain-of-function autoinflammation

    Pulmonary lung fibrosis is a poorly understood process that can arise in pediatric patients with gain-of-function mutations that disrupt the regulation of the cytosolic double stranded DNA sensing pathway, cGAS-STING. This project will define the role that B cells play in mediating lung fibrosis in a mouse model of STING gain-of- function autoinflammation that recapitulates a human disease known as STING Associated Vasculopathy with onset in Infancy (SAVI). The expectation is that the results of these studies will offer insights into the mechanisms by which B cell contribute to fibrotic lung disease and assess, using murine models, whether targeting B cells is a valid strategy for prophylactically treating lung fibrosis.

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IMP graduates pursue both academic and industry career tracks.  In fact, one recent graduate has pursued both, with an academic postdoc, supported by an EMO Fellowship, at the CMM in Vienna and then founded a biotech startup, Allcyte, where he is currently serving as CSO.  Many other graduates take positions directly after completing their degree in the local biopharma industry where expertise in immunology is in high demand. For example, some of our recent graduate have joined Amgen, Pfizer, Sanofi, AstraZeneca, Moderna, and Genetech.  Others have pursued careers in intellectual property and the law, for example at Lathrop GPM.  Another recent graduate joined the Massachusetts Department of Public Health where he manages a team providing surveillance for insect vectored virus.