Upon TLR9 signaling, CD5+ B cells control the IL-12-dependent Th1-priming capacity of neonatal DCs.

The susceptibility to infections and the strong Th2 bias observed in neonates are thought to be due to the immaturity of the dendritic cell (DC) compartment. We show that neonatal DCs, like their adult counterparts, elicit Th1 responses. We also demonstrate that during potentially harmful systemic inflammation, after Toll-like receptor (TLR) 9 triggering, neonatal B cells produce high concentrations of IL-10, preventing optimal IL-12 secretion by neonatal DCs and, thus, Th1 priming. Although both CD5+ and CD5- B cell subsets respond to CpG ODN stimulation, we found that only CD5+ B cells produce IL-10. Therefore, these results show the regulatory role of CD5+ B cells on DC activation in vivo for Th1/Th2 polarization and highlight the paradoxical effects of TLR triggering in vivo.