Biology subjects

Owen, J. C.

Publications and source records attributed to Owen, J. C..

2 recordsLinked to original sources

bioRxiv2026

A transient CD87-centred axis enhances the Th17 potential of cDC2 in neonates

Type 2 conventional dendritic cells (cDC2) orchestrate T cell immunity, yet the signals that regulate their tissue-specific functions across development remain poorly defined. We demonstrate that splenic cDC2/DC3 subset heterogeneity is established perinatally and that splenic ESAMhi cDC2A undergo a transcriptional and functional transition around the time of weaning, which occurs independently of microbiota. Comparative transcriptomics identified neonatal-specific regulatory programs, including elevated expression of Plaur, encoding CD87/uPAR. CD87 sensitizes neonatal ESAMhi cDC2A to coagulation factor XII (FXII), thereby enhancing their capacity to promote Th17 differentiation. In human infants, CD87 expression was high on cDC2, its expression declined with age and in plasma of preterm infants CD87 positively correlated with Th17-associated cytokines. Together, we identify a conserved link between coagulation pathways and cDC2 developmental programming that may offer new opportunities to modulate Th17 responses in infancy. SummarySplenic cDC2 undergo a transcriptional and functional remodeling around weaning. Elevated CD87 expression on neonatal cDC2 enhances their FXII-driven Th17 potential. Conserved in human infants, elevated CD87 expression reveals a coagulation-linked pathway shaping early-life dendritic cell function and suggests targets to improve vaccination.

immunology↗

bioRxiv2021

Differential gene expression reveals host factors for viral shedding variation in mallards (Anas platyrhynchos) infected with low-pathogenic avian influenza virus

Intraspecific variation in pathogen shedding impacts disease transmission dynamics; therefore, understanding the host factors associated with individual variation in pathogen shedding is key to controlling and preventing outbreaks. In this study, ileum and bursa of Fabricius tissues of mallards (Anas platyrhynchos) infected with low-pathogenic avian influenza (LPAIV) were evaluated at various post-infection time points to determine genetic host factors associated with intraspecific variation in viral shedding. By analyzing transcriptome sequencing data (RNA-seq), we found that LPAIV-infected mallards do not exhibit differential gene expression compared to uninfected birds, but that gene expression was associated with viral shedding quantity early in the infection. In both tissues, immune genes were mostly up-regulated in higher shedding birds and had significant positive relationships with viral shedding. In the ileum, host genes involved in viral cell entry were down-regulated in low shedders one day post-infection (DPI), and host genes promoting viral replication were up-regulated in high shedders on two DPI. Our findings indicate that viral shedding is a key factor for gene expression differences in LPAIV-infected mallards, and the genes identified in this study could be important for understanding the molecular mechanisms driving intraspecific variation in pathogen shedding.

genomics↗