About

Jennifer J. Sun is an assistant professor in the Department of Computer Science at Cornell University. Her research develops AI for scientists to accelerate discovery across fields. Her group works with researchers and domain experts to build approaches that enable new ways to collaborate between human experts and machine learning systems. Her work intersects different areas of computer vision and machine learning, including representation learning, program synthesis, generative modeling, and human-AI collaboration. Sun received her Ph.D. in computing and mathematical science from the California Institute of Technology and her bachelor's degree in engineering science (electrical and computer engineering) from the University of Toronto.

Research topics

• Biology
• Immunology
• Virology
• Neuroscience
• Biochemistry
• Literature
• Genetics
• Medicine
• Cell biology
• Philosophy
• Art
• Environmental ethics

Selected publications

• TOX drives CD4+ TH1 effector function, antitumor immunity and autoimmune pathology

  Nature Immunology · 2026-02-27 · 3 citations

  article
  PublisherDOI

• Molecular determinants of NK cell memory

  Trends in Immunology · 2026-03-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Stepwise epigenetic signal integration drives adaptive programming of cytotoxic lymphocytes

  Immunity · 2026-01-30 · 1 citations

  articleSenior author
  PublisherDOI

• RAG suppresses group 2 innate lymphoid cells

  eLife · 2025-04-16

  preprintOpen access

  Abstract Antigen specificity is the central trait distinguishing adaptive from innate immune function. Assembly of antigen-specific T cell and B cell receptors occurs through V(D)J recombination mediated by the Recombinase Activating Gene endonucleases RAG1 and RAG2 (collectively called RAG). In the absence of RAG, mature T and B cells do not develop and thus RAG is critically associated with adaptive immune function. In addition to adaptive T helper 2 (Th2) cells, group 2 innate lymphoid cells (ILC2s) contribute to type 2 immune responses by producing cytokines like Interleukin-5 (IL-5) and IL-13. Although it has been reported that RAG expression modulates the function of innate natural killer (NK) cells, whether other innate immune cells such as ILC2s are affected by RAG remains unclear. We find that in RAG-deficient mice, ILC2 populations expand and produce increased IL-5 and IL-13 at steady state and contribute to increased inflammation in atopic dermatitis (AD)-like disease. Further, we show that RAG modulates ILC2 function in a cell-intrinsic manner independent of the absence or presence of adaptive T and B lymphocytes. Lastly, employing multiomic single cell analyses of RAG1 lineage-traced cells, we identify key transcriptional and epigenomic ILC2 functional programs that are suppressed by a history of RAG expression. Collectively, our data reveal a novel role for RAG in modulating innate type 2 immunity through suppression of ILC2s.

  PublisherDOI

• STAT3 operates as an inflammation-dependent transcriptional switch

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-28 · 1 citations

  preprintOpen accessSenior author

  Signal transducer and activator of transcription 3 (STAT3) is a key regulator of immune cell function, but its role in lymphocytes remains incompletely understood. Here, we show that STAT3 has a context-dependent function in antiviral natural killer (NK) cells, either promoting or impairing adaptive NK cell responses dependent on the level of inflammation. STAT3 is recruited to distinct genomic sites under homeostatic versus inflammatory environments, where it drives different transcriptional programs. Through this re-localization, STAT3 regulates downstream transcription factors MYB and BLIMP-1 in an inflammation-dependent manner to shape NK cell differentiation under homeostasis and during infection. Thus, STAT3 acts as a transcriptional switch that integrates cytokine signals to control lymphocyte adaptation to different environments. This mechanism highlights how therapeutic interventions targeting STAT3 can result in different outcomes depending on the degree of inflammation. HIGHLIGHTS: STAT3 exerts a context-dependent role on adaptive NK cells during viral infectionSTAT3 modulates IL-15 signaling by competing with STAT5 and regulating MYBHomeostatic versus inflammatory cytokines relocate STAT3 to distinct genomic sitesDownstream transcription factors MYB and BLIMP-1 govern STAT3-dependent differentiation.

  PublisherDOI

• TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells

  Nature Immunology · 2025-08-08 · 1 citations

  articleSenior author
  PublisherDOI

• Author response: RAG suppresses group 2 innate lymphoid cells

  2025-05-06

  peer-reviewOpen access
  PublisherDOI

• An IFN/STAT1/CYBB axis defines protective plasmacytoid DC–neutrophil crosstalk in Aspergillus fumigatus–infected mice

  Journal of Clinical Investigation · 2025-08-05

  articleOpen access

  Aspergillus fumigatus is the most common cause of invasive aspergillosis (IA), a devastating infection in immunocompromised patients. Plasmacytoid DCs (pDCs) regulate host defense against IA by enhancing neutrophil antifungal properties in the lung. Here, we define the pDC activation trajectory during A. fumigatus infection and the molecular events that underlie the protective pDC-neutrophil crosstalk. Fungus-induced pDC activation began after bone marrow egress and resulted in pDC-dependent regulation of lung type I and type III IFN levels. These pDC-derived products acted on type I and type III IFN receptor-expressing neutrophils and controlled neutrophil fungicidal activity and ROS production via STAT1 signaling in a cell-intrinsic manner. Mechanistically, neutrophil STAT1 signaling regulated transcription and expression of Cybb, which encodes one of 5 NADPH oxidase subunits. Thus, the results indicate that pDCs regulate neutrophil-dependent immunity against inhaled molds by controlling local expression of a subunit required for NADPH oxidase assembly and activity in the lung.

  PublisherOA PDFDOI

• Kitlo hematopoietic stem cells exhibit distinct lymphoid-primed chromatin landscapes that enhance thymic reconstitution

  Nature Communications · 2025-07-04 · 5 citations

  articleOpen access

  Abstract Hematopoietic stem cells (HSC) with multilineage potential are critical for T cell reconstitution after allogeneic hematopoietic cell transplantation (allo-HCT). The Kit lo HSC subset is enriched for multipotential precursors, but their T cell potential remains poorly characterized. Using a preclinical allo-HCT mouse model, we demonstrate that Kit lo HSCs provide superior thymic recovery and T cell reconstitution, resulting in improved immune responses to post-transplant infection. Kit lo HSCs with augmented bone marrow (BM) lymphopoiesis mitigate age-associated thymic alterations and enhance T cell recovery in middle-aged mice. Mechanistically, chromatin profiling reveals Kit lo HSCs exhibiting higher activity of lymphoid-specifying transcription factors, such as, ZBTB1. Zbtb1 deletion diminishes HSC engraftment and T cell potential; by contrast, reinstating Zbtb1 in megakaryocytic-biased Kit hi HSCs rescues hematopoietic engraftment and T cell potential in vitro and in vivo. Furthermore, age-associated decline in Kit lo HSCs is associated with diminished T lymphopoietic potential in aged BM precursors; meanwhile, Kit lo HSCs in aged mice maintain enhanced lymphoid potential, but their per-cell capacity is diminished. Lastly, we observe an analogous human BM KIT lo HSC subset with enhanced lymphoid potential. Our results thus uncover an age-related epigenetic regulation of lymphoid-competent Kit lo HSCs for T cell reconstitution.

  PublisherOA PDFDOI

• An activating <i>Stat1</i> mutant disrupts normal STAT4 innate lymphocyte programs during viral infection

  Science Immunology · 2025-05-30 · 2 citations

  article

  Interferonopathies drive autoimmunity but can also impair host responses to pathogens, including viral infections. To better understand viral susceptibility of patients with STAT1 gain-of-function (GOF) mutations, we generated conditional knockin mouse models to elucidate disease mechanisms and relevance of different immune subsets. Virally infected Stat1 GOF mice exhibited impaired early IFN-γ production from innate lymphocytes and lethality because of excess prolonged multicytokine production. The presence of the Stat1 GOF allele resulted in premature usage of interferon-stimulated gene factor 3 (ISGF3) over the normal STAT4–AP-1–dependent transcriptomic program in activated innate lymphocytes. Administration of anti–IFN-γ antibodies in wild-type (WT) mice after infection phenocopied Stat1 GOF mice presenting exaggerated inflammation despite viral control. Conversely, early administration of exogenous IFN-γ to infected Stat1 GOF mice prevented lethality and exaggerated cytokine response. Although Stat1 GOF mutations facilitate IFN-γ–mediated autoimmunity, early IFN-γ responses to viral infection via a normal STAT4 program were impaired, leading to overcompensated inflammatory responses in Stat1 GOF mice.

  PublisherDOI

Recent grants

• NIH Grant R00AI085034

  NIH · $498k · 2012

• The natural killer cell response against mouse cytomegalovirus infection

  NIH · $7.4M · 2023–2027

• Regulation of Nfil3 in innate lymphocyte-mediated host immunity

  NIH · $2.8M · 2017–2022

Frequent coauthors

• Lewis L. Lanier

  University of California, San Francisco

  91 shared

• Colleen M. Lau

  59 shared

• Clair D. Geary

  Kettering University

  39 shared

• Endi K. Santosa

  Cornell University

  34 shared

• Timothy E. O’Sullivan

  University of California, Los Angeles

  34 shared

• Nicholas M. Adams

  New York University

  30 shared

• Michael J. Bevan

  University of Oxford

  27 shared

• Simon Grassmann

  Memorial Sloan Kettering Cancer Center

  26 shared

Education

• Ph.D.

  Cornell University