Events

Charkira Patrick - Graduate Student

 May 07, 2026 @ 12:00 p.m.

Host: Advisors: Collynn Woeller, Ph.D. & Jacques Robert, Ph.D.

Claudia Jakubzick, PhD - Professor of Microbiology and Immunology, Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine

Our work reveals functional heterogeneity in interstitial macrophages (IM), showing that distinct chemokine programs determine where immune cells localize and interact. IM niches support anti-tumor TLS formation and lymphocyte recruitment but also recruit protumorigenic macrophages in the tumor microenvironment. Monocyte-derived DCs migrate to tumor-draining lymph nodes to prime suppressive T cells, and transient CCR5 blockade improves DC-based vaccination. Moreover, NAbs are the engine that starts the innate and adaptive immune process to prevent cancer.

 May 04, 2026 @ 11:00 a.m.

 Medical Center | K-307 (3-6408)

Host: Immunology T32 Students - Sponsored by NIH/NIAID Predoctoral Training Program in Immunology

Molly Niska - Graduate Student

 Apr 30, 2026 @ 12:00 p.m.

 Medical Center | K307

Host: Advisors: Martin Zand, MD, Ph.D.& Tim Mosmann, PhD

Taylor Jones - Graduate Student

 Apr 16, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: David Topham, Ph.D.

Emily Britt - Graduate Student

 Apr 09, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Steve Gill, Ph.D.

Ian Stone - Graduate Student

 Mar 26, 2026 @ 12:00 p.m.

 Medical Center | M307 (3-6408)

Host: Advisor: Carlos Díaz-Balzac, M.D., Ph.D.

Ashay Narayana - Graduate Student

 Mar 12, 2026 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Advisor: Brian Ward, Ph.D.

Emma Tonetti - Graduate Student

 Mar 05, 2026 @ 12:30 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Kirsi Järvinen-Seppo, M.D., Ph.D.

Riley Steel - Graduate Student

 Mar 05, 2026 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Advisor: Brian Ward, Ph.D.

Tyler Smith - Graduate Student

The small intestine is a highly dynamic organ that depends on tightly coordinated interactions among the epithelium, immune compartment, and microbiota to support nutrient absorption and immune tolerance. While several pro-inflammatory cytokines, including TNF, IL-17, and IFN-g, play well-established roles during acute intestinal inflammation, their long-term effects on intestinal tissue maintenance and homeostasis remain poorly understood.

Our laboratory has previously shown that infection with the intracellular parasite Toxoplasma gondii triggers a potent IFN-g–mediated acute inflammatory response characterized by epithelial cell damage, dysbiosis, and cell death. Whether the small intestine can fully return to a homeostatic state following resolution of inflammation, or instead retains a long-term imprint of IFN-g–induced cellular perturbations, remains unknown. Using single-nucleus transcriptomic and metagenomic approaches, we found that exposure to a common intracellular pathogen results in long-term epithelial remodeling in the small intestine, characterized by reduced absorptive capacity, partial loss of epithelial stem cells, and a shift toward more mature enterocyte states. These data suggest the presence of a durable epithelial imprint that may underlie chronic malabsorption and altered host–microbiota interactions.

The next goal of this project is to define the molecular mechanisms by which IFN-g exposure reprograms the small intestinal mucosa and to determine how these changes are linked to microbiota composition and function. 

 Feb 26, 2026 @ 12:30 p.m.

 Medical Center | K-307 (3-6408)

Host: Advisor: Felix Yarovinsky, M.D.

Shelby Peres - Graduate Student

The non-tuberculosis mycobacterium (NTM) M. abscessus (Mab) is an opportunistic pathogen increasingly causing disease in humans, especially in patients with immunocompromised conditions such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). The underlying mechanisms of infection between the host and pathogen are less well characterized for NTMs than for M. tuberculosis, leaving a gap in research. Mice typically clear Mab infection quickly, even in IFNγ knockout models; thus, they cannot be used to study chronic infection. Zebrafish lack functional lungs and have a limited adaptive immune response. Therefore, an alternative animal model is needed. We have developed Xenopus tadpoles as a comparative experimental organism to investigate chronic infection relevant to human health. Xenopus tadpoles display a functional immune system, with lungs, T cells dominated by innate-like T cells, and macrophages, making them a reliable model for persistent Mab infection and pathogenesis. Shotgun sequencing performed by Ripoll et al. in 2009 detailed the Mab genome that allowed us to identify a novel putative secondary metabolite pathway encoded in a gene cluster spanning MAB_0284c to MAB_0305 with strong homology to Streptomyces clusters that produce bioactive compounds such as streptonigrin, calcimycin, and nybomycin pathways that produce secondary metabolites.  In collaboration with the Pavelka Lab, we constructed a series of mutant strains, designated Secondary Metabolite Gene Cluster (SMGC) mutants, to investigate the role of the end product, PhzC. These include a deletion mutant of PhzC (∆phzC), its revertant control, and a strain overexpressing a putative positive regulator (ΔcdaR) of the SMGC.

We used our established tail wound inoculation assay, combined with intravital confocal microscopy, to show that ΔphzC mutants impaired macrophage recruitment and reduced macrophage infection in tadpoles compared to WT bacteria. Moreover, preliminary data suggest a lower colocalization rate between the ΔphzC mutant Mab and macrophages as early as 1-day post-infection, and that in vitro, macrophages infected with ΔphzC Mab exhibit increased survival compared to those infected with WT Mab.

These data underscore the utility of Xenopus tadpoles as a model for identifying genetic determinants of Mab immunopathogenesis and suggest a role for this previously uncharacterized pathway. Based on previous work from our lab, we hypothesize that this putative secondary metabolite pathway in the opportunistic pathogen Mab encodes a virulence factor that increases macrophage recruitment to the site of infection, stimulates the innate immune response, and promotes intracellular survival during the initial stages of infection.

 Feb 26, 2026 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Advisor: Jacques Robert, Ph.D.

Maria Ossa - Graduate Student

 Feb 19, 2026 @ 12:30 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Minsoo Kim, Ph.D.

Jesse Jenkins - Graduate Student

 Feb 19, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Ruth Serra-Moreno, Ph.D.

Kei Brown - Graduate Student

BST2 is a potent mammalian antiviral factor that restricts the viral release and enhances immune recognition of a wide array of enveloped viruses, including SARS-CoV-2. It primarily functions through its secondary structure, which prevents the release of nascent virions by tethering them to the host cell surface. Consequently, many of these enveloped viruses have evolved mechanisms to counteract BST2. The ability to overcome BST2 restriction has proven critical, especially for the successful spread of zoonoses like pandemic HIV-1. Whether or not BST2 also serves as a cross-species barrier for coronaviruses, many of which lie in the bat virus reservoir, remains unknown. We plan to fill this gap in knowledge by using the readily available SARS-CoV-2, a now human-adapted virus that is thought to have arisen in bats.

Our lab has recently identified the Spike as SARS-CoV-2’s main antagonist of human BST2 (hBST2), where it downregulates the protein via lysosomal degradation. Further, we identified an accumulation of mutations in the Spike of recent SARS-CoV-2 VOC that have resulted in improved efficiency of hBST2 downregulation compared to ancestral SARS-CoV-2 strains. Although this indicates evolution to counteract hBST2, whether human and bat BST2 can restrict bat coronaviruses is unknown. Many facets of the bat-human cross-species barrier remain to be assessed and could provide valuable knowledge to inform future therapeutics and identify bat coronaviruses poised to cross this barrier.

Here, we aim to answer if coronavirus antagonists of BST2 are species-specific and if BST2 is a driving factor of coronavirus evolution to address our broader question of BST2’s role in the bat-human cross-species barrier for bat coronaviruses. Thus far, we have found that SARS-CoV-2 Wuhan Spike, an ancestral strain, downregulates bat BST2s more efficiently than SARS-CoV-2 Omicron Spike, a recent VOC, via transfection. We also found that RaTG13 (a bat coronavirus closely related to SARS-CoV-2) Spike appears to downregulate Rhinolophus (bat) BST2s to a greater extent than Pteropus (bat) or human BST2. Unexpectedly, it also seems that HIV-1’s Vpu, a known antagonist of hBST2, may have the ability to antagonize bat BST2s as well.

 Feb 12, 2026 @ 12:30 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Ruth Serra-Moreno, Ph.D.

Leah Bernstein - Graduate Student

Defective viral genomes (DVGs) are truncated versions of viral genomes, ubiquitously produced during infection with many RNA viruses, including SARS-CoV-2. DVGs are potent stimulators of antiviral interferon responses and promote persistent viral infection. We identify three conserved recombination hotspots for SARS-CoV-2 DVGs. Among them, hotspot B is the most conserved, with a deletion of ORF7, ORF8, and N from its genome. We observed that DVG-B induced a strong interferon response and inhibited standard viral replication in A549 epithelial cells. Given the important role of alveolar macrophages in antiviral defense, immune regulation, and viral persistence in the lung, understanding how DVGs function in this cell type is critical. However, the immunological effects of DVG-B in macrophages remain poorly defined. Using viral titration, immunofluorescence microscopy, and interferon stimulation assays, we showed that SARS-CoV-2 wild type virus caused a productive infection in THP-1 derived macrophages. However, this infection was much delayed and reduced compared to that in ACE-2 A549 epithelial cells. In macrophages, DVG-B fails to trigger the strong interferon response seen in epithelial cells, as observed by weak interferon and interferon-stimulated gene induction despite intact downstream interferon signaling. This cell-type specific difference may allow macrophages to support SARS-CoV-2 persistence in the lung without triggering a robust antiviral response. Ongoing studies involving immunofluorescence imaging must be performed to better understand and visualize the SARS-CoV-2 infection kinetics within macrophages. This research aims to address a critical gap in knowledge about macrophage function during viral infection, to ultimately improve patient outcomes.

 Feb 12, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Yan Sun, Ph.D.

Zhinian Zhou - Graduate Student

The Orthopoxvirus genus includes several human pathogens: variola virus, which causes smallpox, and emerging pathogens such as monkeypox and borealpox. Vaccinia virus (VACV) is the prototypical orthopoxvirus, and its replication produces intracellular mature viruses (IMVs). A subset of IMVs is further enveloped at the trans-Golgi network (TGN) to form intracellular enveloped viruses (IEVs). IEVs are transported to the plasma membrane and released from infected cells, forming extracellular viruses (EVs). The formation of EVs during VACV infection is required for viral spread. However, the molecular mechanism of EV morphogenesis is not fully understood. The viral protein F13 localizes at the TGN and plays a critical role in the intracellular envelopment of IMVs to form IEV/EVs. Deletion of F13 results in a significant decrease in EV formation and a small plaque phenotype. To better understand the F13’s role in intracellular envelopment, we used Bio-ID to identify proteins that interact with F13 via proximity-dependent biotinylation. Bio-ID identified 125 proteins as significant hits, including EpsinR, which mediates retrograde trafficking from early endosomes (EE) to the TGN. A previous study found that trafficking of F13 to the TGN is required for efficient EV production. EpsinR and the AP-1 complex are both involved in the incorporation of cargo into clathrin-coated vesicles for transport to the TGN. To investigate the factors involved with F13 intracellular localization to the site of wrapping, I used siRNA to deplete EpsinR during infection. While EpsinR was significantly reduced, there was no significant effect on viral spread or F13 localization. Next, I will investigate the role of AP-1 and clathrin in F13 trafficking to the TGN. BioID also identified the conserved orthopoxvirus protein VACVWR161 as a significant hit. Immunofluorescence staining of epitope-tagged VACWR161 found that it colocalizes with F13. However, deletion of VACWR161 did not significantly affect viral spread in BSC40 cells or MRC5 cells. Future studies will use primary keratinocytes, a more physiologically relevant model, to investigate the role of VACWR161 in EV production and pathogenesis.

 Feb 05, 2026 @ 12:00 p.m.

 Medical Center | K-307 (3-6408)

Host: Advisor: Brian Ward, Ph.D.

Zhewen (Kevin) Li - Graduate Student

Acute myeloid leukemia (AML) is an aggressive hematologic malignancy driven by somatic mutations in hematopoietic stem and progenitor cells, resulting in uncontrolled myeloid proliferation and impaired normal hematopoiesis. Despite advances in treatment, curing AML remains challenging, as allogeneic hematopoietic stem cell transplantation—where donor T cells recognize AML cells as “non-self” target—remains the only therapy with curative potential. Notably, AML cells actively remodel the bone marrow microenvironment (BMME) by suppressing immune function and promoting immune evasion, which may explain the limited efficacy of immunotherapies such as immune checkpoint blockade and CAR-T cell therapy in AML.

CD8⁺ T cells are among the most potent cytotoxic lymphocytes capable of eliminating malignant cells; however, the mechanisms by which AML escapes CD8⁺ T cell–mediated killing remain poorly understood. In this study, we aim to characterize CD8⁺ T cell phenotypes in advanced AML, defined by approximately 50% leukemic burden in the bone marrow, and to identify potential targets to restore CD8⁺ T cell function. Based on clinical observations, we hypothesized that CD8⁺ T cells become exhausted and dysfunctional within the AML BMME. Using flow cytometry, we found that CD8⁺ T cells from AML-bearing mice exhibit persistent expression of TOX, a key transcriptional regulator of T cell exhaustion, along with increased expression of inhibitory and dysfunction-associated receptors including PD-1, TIM-3, and KLRG-1. These results suggest potential exhaustion phenotypes. To further define the transcriptional and functional states of these cells and to uncover therapeutic vulnerabilities, we plan to integrate single-cell RNA sequencing with functional assays. Together, this work aims to advance our understanding of CD8⁺ T cell dysfunction in AML and inform strategies to reinvigorate anti-leukemic immunity.

 Jan 29, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisors: Benjamin J. Frisch, Ph.D. and Scott Gerber, Ph.D.

Sophie Troyer - Graduate Student

Childhood food allergy and atopic disease are becoming increasingly prevalent.  A significant goal in this field is to prevent food allergy development and halt the atopic march— the sequential progression of atopic diseases from atopic dermatitis (AD) and food allergy (FA) to asthma and allergic rhinitis. To do this, a greater understanding of the development of allergy in infancy is needed. Communities with farming lifestyles such as the Old Order Mennonite (OOM) community have decreased prevalence of allergic diseases and therefore serve as a model population for protection against allergic diseases. Studies have shown differences between farming and nonfarming communities in the innate immune system such as TLR expression that could explain an immune protective impact of farm exposure and may be due to the differing endotoxin levels and microbiota exposures. This suggests a role for trained immunity which posits that the innate immune system can be trained to respond differently upon re-exposure. To further explore this area of research, we will examine differences in innate immune response between the local OOM infant population and the Rochester urban/suburban infant population (ROC), which comprise our ZOOM1 cohort. To compare innate immune responses, we compare cytokine output of CBMCs and PBMCs after stimulation with various TLR agonists including LPS (TLR4 agonist, bacterial), and ssRNA40/LyoVec (TLR 7/8 agonist, viral). Thus far, we have optimized several stimulation conditions, including TLR agonist concentration, duration of stimulation, whether to rest cells before stimulation, and the use of PBMCs vs isolated CD14+ cells. These experiments will aid in understanding the role of innate immunity in farming lifestyle protection against allergic diseases. Additionally, we sought to examine differences between OOM and ROC in key innate immune marker gene expression for TLR 2, TLR 4, TLR 7, TLR 8, and CD14. Utilizing qPCR, we found trends for multiple TLRs between OOM and ROC allergic subgroups. These results suggest prenatal immune training that may be responsible for the farming lifestyle effect.

 Jan 22, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Kirsi Järvinen-Seppo, M.D., Ph.D - Advisor

Adam Tyrlik - Graduate Stident

Bone Marrow Stromal Cells (BMSCs) are non-hematopoietic cells that provide a favorable microenvironment for Hematopoietic Stem Cells and progenitors, producing supportive factors and immunomodulatory cytokines. Dysfunction in BMSCs contributes to the development of Myelodysplastic Syndrome (MDS), a marrow failure syndrome that may progress to high-risk leukemia. The extreme mutational heterogeneity of MDS, with more than 100 mutations identified, often in combination, represents a major therapeutic challenge. Therefore, conserved MDS-induced BMSC changes would represent appealing treatment targets. In this study, we isolate Lineage- CD271 (NGFR)+ BMSCs from healthy and MDS human bone marrow aspirates and perform single-cell RNA sequencing, using osteogenic, adipogenic, osteochondral, and fibroblastic fate-associated genes to identify three major, previously described BMSC populations. We then identify a distinct subset of BMSCs with significant upregulation of hematopoietic support genes, including CXCL12, CSF1, LEPR, and VCAM1, indicating BMSCs more likely to be engaged in hematopoietic support. Based on transcriptional data we demonstrate a broad, conserved change in immunomodulatory capacity, and a loss of heterogenicity in this Supportive population across multiple mutationally heterogenous MDS patients. Utilizing an extended sorting strategy that includes CD106 (VCAM1) and CD146 (MCAM) in addition to CD271, we sorted both CD271+CD146-CD106- (NLC) and CD271+CD146+CD106+ (NVML) cells. With RNA sequencing we demonstrate that this sorting strategy isolates distinct populations, and that NVML cells are transcriptionally similar to the Supportive BMSC population identified by single cell RNA seq based on fate associated gene expression and MDS associated transcriptional changes. We then show that, when functionally compared to the NLC population, sorted NVML cells have higher adipogenic and chondrogenic differentiation capacity, increased mitochondrial membrane potential and increased capacity for support of bone marrow from healthy controls, while the capacity to provide hematopoietic support is diminished in the context of MDS. To identify how the MDS associated changes within BMSCs translate to changes in BMSC and hematopoietic stem cell (HSC) interaction, we performed an computational predicted interaction analysis between MDS and healthy control derived BMSCs and CD34+ Human Bone Marrow fraction from MDS patients as well as healthy controls.

 Jan 15, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Laura M. Calvi, M.D.

Zirui Zhao - Graduate Student

The rise of antibiotic resistance is a critical global health challenge, underscoring the urgent need for novel strategies to re-sensitize resistant bacteria to treatment. Current antibiotic research approaches primarily rely on growth inhibition as the key metric for drug discovery and resistance assessment. However, emerging evidence suggests that bacterial metabolism, independent of growth, both influences and is influenced by antimicrobial resistance (AMR), revealing a potential new therapeutic avenue. However, despite its significance and potential clinical utility, the relationship between antibiotic resistance and metabolism remains poorly understood. To better understand how metabolic adaptations contribute to AMR, we examined the metabolic dependencies of various antibiotics across multiple Staphylococcus aureus strains, including methicillin-resistant (MRSA) and methicillin-susceptible (MSSA) clinical isolates. Susceptibility profiling confirmed that a strain’s antibiotic susceptibility can be modulated by altering its metabolism, achieved by supplementing it with various metabolites, and highlighted some specific metabolite-drug combinations for further investigation. Here, I focus on oxacillin and adenine as a representative case to probe how metabolic state alters drug susceptibility, since beta-lactams remain a first-line therapy for Staphylococcus aureus infections and adenine produced a strong but nonuniform effect across isolates. Adenine similarly altered susceptibility to multiple beta-lactam antibiotics across an expanded panel of MRSA and MSSA strains. Importantly, this response did not segregate by MRSA versus MSSA classification, but rather varied at the individual strain level, revealing a strong strain-specific metabolic control of beta-lactam sensitivity. These findings suggest that differences between strains, rather than resistance class alone, could guide a more personalized approach to antibiotic therapy. Ongoing work involves mechanistic investigation into the mechanism underlying the adenine strain-specific effect on beta-lactam drugs, including ATP, c-di-AMP, and adenine pathway-associated gene expression level measurement.

 Jan 08, 2026 @ 12:00 p.m.

 Medical Center | K307 (3-6408)

Host: Advisor: Allison Lopatkin, Ph.D.