Infants are easy targets for viruses and bacteria, as their immune responses lack the punch to ward off pathogens. Zhang et al. (page 1107) now find that young immune systems are well developed but are sabotaged by a group of childish B cells.
In adults, microbes trigger defense responses by activating Toll-Like Receptors (TLRs) on dendritic cells (DCs). The DCs then ramp up defense by secreting Interferons 
and ß (IFN /ß), which are toxic to pathogens, and pro-inflammatory TNF and interleukin-12 (IL-12), which reinforce inflammation by activating T cells.
In newborns, however, TNF and IL-12 are only weakly produced during inflammation, even though neonatal DCs produce these cytokines when stimulated in vitro. To identify the in vivo roadblock, Zhang et al. focused on the anti-inflammatory cytokine IL-10, as it is a known inhibitor of TNF and IL-12 production. In an earlier study, the group found that IL-10 is produced by a subset of B cells that are more abundant in newborns than in adults.
The team now shows that these B cells overwhelm inflammatory responses in newborn mice. Pathogens triggered TLRs on both B cells and DCs. The B cells responded by producing IL-10, while the DCs made IFN/ß. But instead of stoking inflammation, the IFN/ß enhanced B cell IL-10 production, which then blocked DC secretion of TNF/IL-12. This regulatory loop sabotaged anti-microbial immunity in newborns, but it also had a positive effect: it allowed young mice to avoid overenthusiastic and potentially lethal inflammatory responses. The team speculates that this mechanism might also prevent human infants from succumbing to inflammation. Adults do not get the same benefit, as their IL-10-secreting B cells are vastly out-numbered by inflammatory DCs. 
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