Neonatal Immune Cells Use Coagulation Pathway to Enhance Th17 Response, Study Finds
Researchers have identified a transient molecular axis in neonatal dendritic cells, centered on the protein CD87, that enhances the capacity to drive Th17 immune responses in early life. The study found that splenic cDC2 dendritic cells undergo a developmental transition around weaning, with CD87 expression declining with age in both mice and human infants. This conserved link between coagulation pathways and early immune programming may open new avenues for modulating inflammatory responses in neonates and preterm infants.
A new preprint study published on bioRxiv reports that type 2 conventional dendritic cells (cDC2) in the spleen establish their functional heterogeneity around the time of birth, with a specific subset—ESAMhi cDC2A—undergoing a transcriptional and functional shift near weaning that occurs independently of gut microbiota. Comparative transcriptomics revealed that neonatal cDC2 specifically upregulate Plaur, the gene encoding the surface receptor CD87 (also known as uPAR). CD87 sensitizes these neonatal dendritic cells to coagulation factor XII (FXII), a component of the blood clotting cascade, which in turn amplifies their ability to promote Th17 T cell differentiation—a pathway associated with inflammatory and autoimmune responses. In human infants, CD87 expression on cDC2 was found to be elevated and declined progressively with age, mirroring the mouse findings. In preterm infants specifically, plasma levels of CD87 positively correlated with Th17-associated cytokines, suggesting clinical relevance. The authors propose that this conserved developmental axis between coagulation signaling and dendritic cell programming could represent a therapeutic target for conditions involving dysregulated Th17 immunity in early life.
What's missing
As a preprint, this work has not yet undergone formal peer review, and causal claims—particularly the translational relevance to human preterm infant outcomes—remain to be validated in larger cohorts. The study does not address whether the CD87-FXII-Th17 axis contributes to specific neonatal diseases (e.g., neonatal sepsis, necrotizing enterocolitis, or early-onset autoimmunity), nor whether therapeutic modulation of this pathway is safe or feasible in clinical settings. The mechanistic link between FXII signaling and downstream Th17 polarization within cDC2 is described but the full intracellular signaling pathway remains incompletely characterized.
What different sources said
- bioRxivCenter
A transient CD87-centred axis enhances the Th17 potential of cDC2 in neonates
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