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 a specific dendritic cell subset (ESAMhi cDC2A) undergoes a developmental transition around weaning, with elevated CD87 sensitizing these cells to coagulation factor XII and boosting Th17-promoting activity. The findings reveal a conserved link between coagulation biology and early immune programming that could inform strategies to modulate inflammatory responses in infancy.
A preprint study posted to bioRxiv reports that type 2 conventional dendritic cells (cDC2) in the spleen establish their subset diversity around the time of birth, with a specific subpopulation called ESAMhi cDC2A undergoing a transcriptional and functional shift near weaning. This transition occurs independently of the gut microbiota, suggesting it is driven by intrinsic developmental programming rather than environmental microbial signals. Comparative transcriptomics revealed that neonatal cDC2A uniquely upregulate Plaur, the gene encoding the surface receptor CD87 (also known as uPAR). CD87 renders these cells responsive 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 conditions. In human infants, CD87 expression on cDC2 was found to be elevated and declined with age, and in preterm infants, plasma CD87 levels positively correlated with Th17-associated cytokines, suggesting the mechanism is conserved across species. The authors propose that this coagulation–dendritic cell–Th17 axis may represent a targetable pathway for modulating immune responses in early life, with potential relevance to neonatal inflammatory disease.
What's missing
As a preprint, this work has not yet undergone formal peer review, and causal claims — particularly regarding CD87's role in human neonatal Th17 responses — remain to be independently validated. The study does not address whether the elevated Th17 potential in neonates is pathological or physiologically beneficial, nor does it clarify the clinical conditions under which FXII-CD87 signaling might be therapeutically targeted. The correlational data from preterm infants cannot establish causality, and the preterm population may not be representative of healthy neonatal immune development.
What different sources said
- bioRxivCenter
A transient CD87-centred axis enhances the Th17 potential of cDC2 in neonates
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