About

Jennifer Elisseeff is the F. Stuart Hodgson Department Head of the Department of Chemical and Biomolecular Engineering at Johns Hopkins University, with an appointment in the Department of Biomedical Engineering. She is the founder of the Translational Tissue Engineering Center at the Johns Hopkins Department of Biomedical Engineering and the Wilmer Eye Institute, where she served as director from 2010 until 2023. Elisseeff is a pioneer in the development and commercial translation of injectable biomaterials for regenerative therapies. Her research areas include regenerative immunology, biomaterials, aging, and arthritis. She is the first Johns Hopkins faculty member to be elected to all three national academies—the National Academy of Engineering, the National Academy of Medicine, and the National Academy of Science. Elisseeff serves on the scientific advisory boards of Bausch and Lomb, Kythera Biopharmaceutical, and Cellular Bioengineering Inc. She has received numerous awards, including the Carnegie Mellon Young Alumni Award, Arthritis Investigator Award from the Arthritis Foundation, Yasuda Award from the Society of Physical Regulation in Medicine and Biology, and recognition as a top innovator under 35 by Technology Review magazine. She was elected a fellow in the American Institute for Medical and Biological Engineering and a Young Global Leader in the World Economic Forum. Elisseeff has published over 200 articles, book chapters, and patent applications, and has given more than 130 invited lectures nationally and internationally. She holds a bachelor’s degree in chemistry from Carnegie Mellon University and a PhD in medical engineering from the Harvard-MIT Division of Health Sciences and Technology. Her postdoctoral work included a fellowship at the National Institute of General Medical Sciences Pharmacology Research Associate Program. She joined Johns Hopkins University as an assistant professor in 2001 and has co-founded several startups focused on soft tissue regeneration and wound healing.

Research topics

• Cancer research
• Medicine
• Immunology
• Chemistry
• Pharmacology
• Biology
• Biochemistry
• Cell biology
• Internal medicine
• Pathology

Selected publications

• RNAseq data from the muscle of a C57BL/6 female mouse

  Cellular Senescence Network (SenNet) · 2026-04-15

  datasetOpen access
  PublisherDOI

• RNAseq data from the muscle of a C57BL/6 female mouse

  Cellular Senescence Network (SenNet) · 2026-04-15

  datasetOpen access
  PublisherDOI

• RNAseq data from the muscle of a C57BL/6 female mouse

  Cellular Senescence Network (SenNet) · 2026-04-15

  datasetOpen access
  PublisherDOI

• Regulatory T cells clonally expand and contribute to stromal cell function in fibrotic response to synthetic implants

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-06

  articleOpen accessSenior authorCorresponding

  Fibrosis plays a key role in both chronic disease progression and failure of synthetic biomaterial implants. However, the contribution of adaptive immunity to fibrotic development remains incompletely understood, particularly for regulatory T cells (Tregs). Here, we used single-cell multiomic profiling, integrating transcriptomics with T cell receptor (TCR) sequencing, to map Treg heterogeneity and clonal dynamics in a synthetic material-induced model of fibrosis. We uncovered progressive Treg clonal expansion accompanied by TCR activation signatures and an increasingly immunosuppressive phenotype along a continuous transcriptional trajectory. These Tregs suppressed immune responses and influenced extracellular matrix and vascular gene expression. Cell-cell communication inference predicted Treg-driven activation of pro-fibrotic and vasculogenic transcriptional programs in fibroblasts and endothelial cells, including Sox-family transcription factors. Functional Treg depletion increased inflammation and significantly reduced neovascularization. Together, these findings identify Treg functions in the fibro-vascular niche through stromal cell modulation, highlighting immune-stromal interactions as an important axis in fibrosis.

  PublisherOA PDFDOI

• 3D, multi-omic imaging reveals molecular biomarkers of the pre-metastatic niche in lung cancer

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-18

  articleOpen access

  Abstract The recurrence rate following complete surgical resection of primary non-small cell lung cancer is as high as 55%, yet no approach currently exists to evaluate the risk of local recurrence. The premetastatic paradigm is the recognition that metastasis is preceded by reprogramming naïve tissues to prime a microenvironment for tumor cell survival and subsequent reactivation. Identification of biomarkers of the pre-metastatic niche would allow us to evaluate a patient’s risk of local relapse in the normal lung parenchyma surrounding the resected tumor. We designed a workflow incorporating in vivo modelling, radiology, and deep learning-guided three-dimensional (3D) imaging, spatial proteomics, and transcriptomics to identify previously unreported signals associated with the early transformation of the lung parenchyma announcing regional metastasis. We curated biorepository spanning timepoints before and after resection of primary Lewis Lung Carcinoma (LLC) tumors. Using radiology and cellular resolution 3D histology, we calculated the number and distribution of metastases in mouse lungs and developed an algorithm to guide placement of spatial proteomics and transcriptomics to regions containing early micro-metastases and the pre-metastatic microenvironment. Molecular and tissue features associated with presence, size, and location of metastases guided the identification of both myeloid (F4/80) and senescent (p16/p21) cell signatures in the premetastatic and metastatic environments. Finally, multiparametric flow cytometry of metastatic lungs in a senescence reporter GEMM (tdTomato-p16 INKA mice) resolved senescent cells including alveolar macrophages as the cellular phenotypes associated with these early premetastatic signatures. Altogether, this work highlights a novel AI-assisted approach for detection of biomarkers of tissue remodeling during lung cancer invasion.

  PublisherOA PDFDOI

• Antibiotic-induced microbiota depletion impairs the pro-regenerative response to a biological scaffold in mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-27 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Abstract Therapeutic biological scaffolds promote tissue repair primarily through the induction of type 2 immunity. However, systemic immunological factors–including aging, sex, and previous infections–can modulate this response. The gut microbiota is a well-established modulator of immune function across organ systems, yet its influence on type 2-mediated repair remains underexplored. Here, we establish a bidirectional relationship between the gut microbiota and biological scaffold-mediated tissue repair. Utilizing a conventionalized germ-free mouse, we demonstrate that scaffold implantation induces compositional and functional changes in the gut microbiome, particularly affecting amino acid biosynthesis. Additionally, in a model of antibiotic-induced microbiota depletion (AIMD), we show that dysbiosis disrupts key immune regulators of type 2 immunity, including reductions in eosinophils, pro-regenerative macrophages, and IL-4-producing CD4 + T cells. At 6 weeks post-scaffold implantation, we observed a significant decrease in myocytes with centrally located nuclei alongside an upregulation in pro-fibrotic gene expression with antibiotic treatment. These findings provide insights into the influence of the gut microbiota on type 2-mediated tissue repair. Significance Statement Antibiotics are routinely administered perioperatively to prevent infection during surgeries and biomaterial implantation. Here, we demonstrate that antibiotic-induced microbiota depletion disrupts the type 2 immune response critical for biomaterial-mediated tissue repair. Our findings highlight the gut microbiota as a determinant of constructive healing and a potential contributor to inter-individual variability in responses to biologic scaffolds.

  PublisherOA PDFDOI

• Higher levels of VEGF-A and TNFα in patients with immune checkpoint inhibitor-induced inflammatory arthritis

  Arthritis Research & Therapy · 2025-04-01 · 4 citations

  articleOpen access

  BACKGROUND: Immune checkpoint inhibitors (ICI), a type of cancer immunotherapy, can cause side effects including inflammatory arthritis (ICI-IA). Previous studies of ICI-IA do not include a thorough characterization of associated immune responses to provide potential targets for treatment. We aimed to identify cytokines uniquely increased in ICI-IA and determine correlations with IA severity and persistence. METHODS: We evaluated patients diagnosed with ICI-IA by a rheumatologist (n = 80); control serum was obtained from ICI-treated cancer patients without any diagnosed irAEs (n = 17) or diagnosed with an unrelated irAE (n = 19). Serum was assayed to quantify 9 cytokine levels (IFN-γ, IL-4, IL-6, IL-10, IL-12p70, IL-1α, TNF-α, IL-17a, VEGF-A) using MSD U-PLEX assay. Mann-Whitney U tests were performed to evaluate differences in cytokine levels between control and ICI-IA groups. The Kruskal-Wallis test and multivariable ordinal logistic regression were used to determine difference in cytokine levels between patients of differing disease activity. RESULTS: VEGF-A and TNFα were significantly elevated in patients with ICI-IA compared to ICI-controls; results persisted when restricting analyses to patients not treated with immunosuppressants at the time of sampling. ICI-IA patients were stratified by IA severity using CDAI score; there was significantly higher VEGF-A in those with higher disease activity. Ordinal logistic regression showed higher levels of IL-6 and VEGF-A were associated with higher disease activity. CONCLUSION: Elevated levels of VEGF-A and TNFα are associated with ICI-IA. There was also higher IL-6 and VEGF-A among those with higher disease activity when controlling for confounding. These cytokines could be used as biomarkers of ICI-IA severity and present therapeutic targets.

  PublisherOA PDFDOI

• Supplementary Methods and Figures from Transfer Learning Reveals Cancer-Associated Fibroblasts Are Associated with Epithelial–Mesenchymal Transition and Inflammation in Cancer Cells in Pancreatic Ductal Adenocarcinoma

  2025-10-06

  preprintOpen access

  <p>Supplementary methods and figures</p>

  PublisherDOI

• Innate and Adaptive Immune Responses to Clinical Hyaluronic Acid Fillers

  Journal of Cosmetic Dermatology · 2025-07-01 · 5 citations

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Crosslinked hyaluronic acid (HA)-based hydrogels are commonly used as dermal fillers where they interact with surrounding tissues including host stromal and immune cells. HA fillers are widely used for aesthetic applications, with products designed with varying properties depending on their indication. Although HA fillers have been demonstrated to have a strong biocompatibility profile, a small subset of patients' experiences delayed-onset adverse events hypothesized to be inflammatory and allergy-related outcomes such as delayed-onset hypersensitivity. AIMS: The overall goal of this study was to evaluate the innate and adaptive immune response to two clinically available HA filler formulations. METHODS: Using multiparametric flow cytometry, we characterized the immune response to Juvèderm Volbella (VYC-15 L) and Juvèderm Ultra 3 (SGD-30XP) in a murine quadricep muscle resection that enables implantation of larger volumes and exposure to muscle and adipose. RESULTS: Presence of the implanted HA filler increased recruitment of immune cells, specifically antigen presenting macrophages, eosinophils, and gamma-delta (γδ) T cells to the injury site compared to no implant (saline) controls. Comparing the two materials, VYC-15 L increased interleukin 17a (IL17a) production by lymphocyte subsets at the injury site and induced higher levels of circulating IgE relative to SGD-30XP and saline controls. CONCLUSION: Overall, these results provide insights into the immune response to HA fillers and how different formulations may alter the immune outcomes.

  PublisherOA PDFDOI

• γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response

  Nature Communications · 2025-10-02 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Abstract Immune-stromal crosstalk governs tissue fibrosis, which is marked by dysregulated extracellular matrix (ECM) production and aberrant vasculature. Here, we investigate how γδ T cell interactions with stromal cells shape fibrosis in the foreign body response. During the acute reaction, type-1 (γδIFNγ) and type-17 (γδ17) effector subsets accumulated at the implant. While γδIFNγ decreased as fibrosis progressed, activated γδ17 persisted as dominant interleukin-17 producers. The γδ17 increased with aging and high-fat diet, both factors associated with chronic inflammation and fibrosis. Co-culture with γδ17 stimulated fibroblast expression of collagen genes and intercellular communication inference linked γδ T cell ligands to activation of ECM remodeling and vascular development programs in fibroblasts and endothelial cells. Finally, genetic deletion of γδ T cells altered expression of ECM components and increased vessel size within the fibrotic matrix. Altogether, our findings implicate γδ T cells in regulating stromal behavior to modulate composition and vascularity of fibrotic tissues.

  PublisherOA PDFDOI

Recent grants

• Single cell characterization of the biomaterial immune and stromal response

  NIH · $2.5M · 2020–2025

• Biomaterials-directed regenerative immunotherapies

  NIH · $5.7M · 2019–2025

• NIH Grant R01AR054005

  NIH · $2.5M · 2015

• Develop BCL-xL proteolysis targeting chimeras as safer and better senolytics

  NIH · $2.6M · 2019–2025

• NIH Grant R21EB002369

  NIH · $409k · 2005

Frequent coauthors

• Drew M. Pardoll

  Johns Hopkins University

  164 shared

• Franck Housseau

  Sidney Kimmel Comprehensive Cancer Center

  159 shared

• Liam Chung

  Johns Hopkins University

  146 shared

• Matthew T. Wolf

  National Cancer Institute

  132 shared

• Elana J. Fertig

  Sidney Kimmel Comprehensive Cancer Center

  123 shared

• Ada Tam

  Johns Hopkins University

  122 shared

• Kaitlyn Sadtler

  National Institute of Biomedical Imaging and Bioengineering

  114 shared

• David R. Maestas

  University of Pittsburgh

  89 shared

Labs

• Elisseeff LabPI

  Not provided

Awards & honors

• Carnegie Mellon Young Alumni Award
• Arthritis Investigator Award from the Arthritis Foundation
• Yasuda Award from the Society of Physical Regulation in Medi…
• Top Innovator Under 35 by Technology Review magazine (2002)
• Top 10 Technologies to Change the Future by Technology Revie…