About

Kellie Ann Jurado, PhD, is a Presidential Assistant Professor at the University of Pennsylvania Perelman School of Medicine. She is a member of the Institute for Immunology and the Penn Center for Research in Reproduction and Women’s Health. Her research focuses on studying early life immunity using emerging viruses, with the goal of uncovering basic immunobiological mechanisms that regulate immune responses in utero and during early life. Her work investigates immune system function, regulation, and development during pregnancy and in neonates under both healthy and inflammatory conditions, leveraging emerging viruses as biological probes to decode early life immunity. Her research aims to describe fundamental immunobiology and identify opportunities to improve offspring health outcomes by understanding molecular mechanisms involved in fetal immune system development.

Research topics

• Biology
• Virology
• Immunology
• Biochemistry
• Medicine
• Cell biology
• Pharmacology
• Genetics

Selected publications

• Acute Paternal Immune Activation Shapes Embryonic Development and Protects Offspring from Viral Infection

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-10

  articleOpen accessSenior authorCorresponding

  The evolutionary arms race between host and pathogen is traditionally framed as a multigenerational paradigm, where beneficial host immune adaptations accrue in a population over time through DNA sequence variation. If pathogens exposure alters epigenetic information inherited by offspring through paternal gametes, advantageous immune traits could emerge within a single generation. We show that acute paternal immune activation (PIA) induces immune signaling in the male reproductive tract and remodels the sperm small RNA profile. Using IVF, we show that altered sperm small RNAs from immune-activated males reprograms gene expression in preimplantation embryos, eliciting sex-specific transcriptional responses. This transcriptional program is reflected in a striking inherited phenotype, as male offspring sired by PIA males exhibit enhanced survival following lethal viral challenge. These findings identify sperm small RNAs as a molecular mechanism that links PIA to embryonic development and offspring immunity, providing a comprehensive framework for how PIA shapes inherited pathogen protection.

  PublisherOA PDFDOI

• Acute Paternal Immune Activation Shapes Embryonic Development and Protects Offspring from Viral Infection

  SSRN Electronic Journal · 2026-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface

  Nature Communications · 2025-12-19 · 1 citations

  articleOpen accessSenior author

  Congenital viral infections can have severe consequences for pregnancy and fetal outcomes. Remarkably, the fetal-derived placenta serves as a robust barrier to infection through meticulous regulation by immune effectors and cytokines. Yet, the regulatory roles of many cytokines remain undefined at the maternal-fetal interface, including Interleukin-27 (IL-27). Here, we show that trophoblast organoids derived from human placentas constitutively express both IL-27 and its receptor, and restrict Zika virus infection through IL-27 signaling. Through bulk RNA-sequencing of trophoblast organoids in the absence and presence of IL-27 signaling, we demonstrate IL-27-mediated upregulation of antiviral genes. Finally, we show that IL-27 signaling is critical to restricting placental viral burdens and protecting against pathologic fetal outcomes during murine congenital Zika virus infection. In this work, we demonstrate a novel role for IL-27 in the placenta and establish IL-27 as an innate antiviral defense at the maternal-fetal interface during congenital viral infection.

  PublisherOA PDFDOI

• Targeting pathogenic interferon-stimulated gene RSAD2 improves pregnancy outcomes in systemic lupus erythematosus models

  Cell Reports Medicine · 2025-03-01 · 2 citations

  articleOpen accessSenior authorCorresponding

  Excessive type I interferons during pregnancy are associated with poor pregnancy outcomes. Ding et al. 1 demonstrate the pathogenic effects of the interferon-stimulated gene RSAD2 that drives adverse pregnancy outcomes through placental lipid accumulation, and further identify a promising therapeutic candidate. Excessive type I interferons during pregnancy are associated with poor pregnancy outcomes. Ding et al. 1 demonstrate the pathogenic effects of the interferon-stimulated gene RSAD2 that drives adverse pregnancy outcomes through placental lipid accumulation, and further identify a promising therapeutic candidate.

  PublisherDOI

• Decoding the immune cells in the fetal brain at murine mid-gestation 4687

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description Adverse events during gestation can influence long-term offspring immunity by disrupting key fetal developmental milestones. Inflammation can alter the emergence of several fetal immune subsets, however, these studies primarily focus on maternal factors that govern development leaving fetal contributions unknown. Fetal immunity is best characterized in context of the liver, the site of fetal hematopoiesis at mid-gestation. We used a high-dimensional sequencing technology, Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq), that allowed us to simultaneously study surface protein markers and gene expression at a single-cell resolution. Interestingly, we identified two multipotent progenitor cell subsets present in the fetal brain at mid-gestation. The presence of progenitor immune cells in the fetal brain highlights its susceptibility to inflammatory events that occur during development. Therefore, we sought to further characterize the phenotype of immune cells in fetal brain with respect to the fetal liver isolated from murine implantation sites at mid-gestation. We identified eleven clusters of immune cells shared by both the fetal brain and liver, ten of which are of innate immune cells at various stages of development, including both multipotent progenitor populations. Our findings provide foundation to understand fetal immune development and will lead to future work studying the consequences of gestational inflammation on the fetal immune system. Funding Sources Howard Hughes Medical Institute through the Gilliam Fellows Program Topic Categories Neuroimmunology (NEUR)

  PublisherOA PDFDOI

• Type I interferon exposure of an implantation-on-a-chip device alters invasive extravillous trophoblast function

  Cell Reports Medicine · 2025-03-01 · 6 citations

  articleOpen accessSenior authorCorresponding

  Inappropriate type I interferon (IFN) signaling during embryo implantation and placentation is linked to poor pregnancy outcomes. Here, we evaluate the consequence of elevated type I IFN exposure on implantation using a human implantation in an organ-on-a-chip device. We reveal that type I IFN reduces extravillous trophoblast (EVT) invasion capacity. Analyzing single-cell transcriptomes, we uncover that IFN truncates invasive EVT emergence in the implantation-on-a-chip device by stunting EVT epithelial-to-mesenchymal transition. Disruptions to the epithelial-to-mesenchymal transition are associated with the pathogenesis of preeclampsia, a life-threatening disorder of pregnancy. Strikingly, IFN stimulation induces genes associated with increased preeclampsia risk in EVTs. These dysregulated EVT phenotypes ultimately reduce EVT-mediated endothelial cell vascular remodeling in the implantation-on-a-chip device. Overall, our work implicates unwarranted type I IFN as a maternal disturbance that can result in abnormal EVT function that could trigger preeclampsia. • Elevated type I interferon (IFN) abrogates extravillous trophoblast (EVT) invasion • EVT exposure to IFNb limits the emergence of invading EVTs • IFN stimulation promotes preeclamptic gene signature in EVTs • EVT-directed vascular remodeling is limited by type I IFN Simoni, Negatu et al. use an implantation-on-a-chip device to evaluate the consequence of elevated type I IFN exposure on implantation. Using single-cell transcriptomes, they uncover that type I IFN exposure alters extravillous trophoblast invasion and induces preeclampsia-associated genes, implicating unwarranted type I IFN as a maternal disturbance that can trigger preeclampsia.

  PublisherDOI

• Paternal immune activation protects offspring from severe disease during viral infection 3329

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description Maternal immune activation during gestation can influence offspring behavior and immunity. However, the influence of paternal immune activation (PIA) on progeny is understudied. Limited evidence indicates that PIA influences offspring behavior via alterations in epigenetic information carried within sperm. Yet, explorations into the impacts of PIA on offspring immunity are minimal. I have shown that PIA with or without viral replication remodels the epigenetic information within sperm by altering the small RNA profile. Moreover, we have demonstrated that PIA alters transcription in the early embryo, downregulating immune regulatory genes. To further explore the impacts of PIA, juvenile offspring from PIA or control males were infected with an adult lethal dose of Influenza A Virus. Offspring sired by PIA males had improved survival and less severe clinical outcomes during infection. Protection did not correlate with lower viral burden in the lungs, leading us to explore differences in immune mediated pathology. Altogether, inflammation in the father alters offspring immunity, providing protection during viral infection. We believe PIA mediated alterations to sperm small RNAs spark differential immune regulation as early as the preimplantation embryo, leading to protection from severe infection within offspring. This paradigm-altering finding uncovers a new mechanism in the evolutionary arms race between host and pathogen wherein immunity can be acquired within one generation. Funding Sources NSF GRFP The PEW Charitable Trust The David and Lucille Packard Foundation Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

  PublisherOA PDFDOI

• Neutral lipid processing in glia is sexually dimorphic and promotes sleep through diacylglycerol catabolism

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-12 · 1 citations

  preprintOpen access

  Abstract Sleep is thought to have a protective role in clearing toxic waste from the brain, which may include processing of damaged lipids. We recently showed that blocking endocytosis in glia increases sleep and report here that this block is associated with an increase in peroxidized lipids and glial lipid droplet accumulation, raising the possibility that accumulation of these lipids increases the need to sleep. Sleep gain induced by blocking glial transport is exaggerated by knockout of the lipid droplet coat protein, Lipid Storage Droplet 2 ( Lsd2 ), suggesting that sleep-promoting lipids are not contained in lipid droplets. To identify lipids regulated by sleep state, we performed global, targeted lipidomics analysis on Drosophila neurons and glia, screening nearly 3,000 lipids across 11 major classes. This revealed that sex influences lipid composition in both cell types and lipid homeostasis following extended wakefulness. Female neurons and glia are enriched in ultra-long chain fatty acids, triacylglycerols, and diacylglycerols, with glial diacylglycerol enrichment correlating with elevated sleep need. Based on manipulations of neutral lipid metabolic pathways, we propose that monoacylglycerols, products of glial diacylglycerol catabolism, promote sleep.

  PublisherOA PDFDOI

• Oropouche virus disrupts neurodevelopment and is vertically transmitted

  Research Square · 2025-09-09 · 1 citations

  preprintOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Interleukin 27 (IL-27) is an antiviral cytokine at the maternal-fetal interface 4478

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description During the critical developmental period of pregnancy, there are substantial consequences to infection. The placenta serves as a robust defense against congenital infection through its constitutive expression of antimicrobial cytokines. IL-27 is a highly expressed cytokine in the placenta, however its functional role at this barrier is unknown. In other contexts, IL-27 is immunoregulatory and is directly antiviral in human keratinocytes. Thus, our objective was to determine how IL-27 contributes to placental immune responses during congenital viral infection. We first utilized a human trophoblast organoid (TO) model to study IL-27 signaling in placental cells. We show that TOs recapitulate placental IL-27 expression in vitro, and that TOs exhibit higher Zika virus (ZIKV) burdens in the absence of IL-27 signaling. To further study placental IL-27 signaling during congenital viral infection, we next utilized an immunocompetent mouse model of congenital ZIKV. We obtained IL-27-deficient dams by routinely treating pregnant mice with IL-27-neutralizing antibody, or by genetic deletion of the IL-27 receptor. We found that infected, IL-27-deficient dams exhibited more pathologic fetal outcomes than control dams, despite similar fetal viral burdens. Interestingly, IL-27-deficient dams had significantly higher placental ZIKV burdens relative to control dams. In summary, these data identify a protective antiviral role for IL-27 in the placenta during congenital viral infection. Funding Sources Supported by NIH/NIAID 1R01AI180138-01, University of Pennsylvania Training Grant T32 GM-07229. Additional funding provided by the Linda Pechenik Montague Investigator Award and the Pew Charitable Trusts Biomedical Scholars Program. Topic Categories Mucosal and Regional Immunology (MUC)

  PublisherOA PDFDOI

Frequent coauthors

• Alan Engelman

  Dana-Farber Cancer Institute

  20 shared

• Seble G. Negatu

  University of Pennsylvania

  16 shared

• Akiko Iwasaki

  Yale University

  13 shared

• Erol Fikrig

  Yale University

  12 shared

• Peter Hewins

  University of Pennsylvania

  12 shared

• Christine Vazquez

  University of Pennsylvania

  12 shared

• Jörg Bürger

  Humboldt-Universität zu Berlin

  12 shared

• Ida Vang Andersen

  University of Copenhagen

  11 shared