Abstract
In comparison to adults, newborns display a heightened susceptibility to pathogens and a propensity to develop allergic diseases. Particular properties of the neonatal immune system can account for this sensitivity. Indeed, a defect in developing protective Th1-type responses and a skewing toward Th2 immunity characterize today the neonatal T-cell immunity. Recently, new findings concerning Th17, regulatory helper T-cell, and follicular helper T-cell subsets in newborns have emerged. In some circumstances, development of effector inflammatory Th17-type responses can be induced in neonates, while differentiation in regulatory T-cells appears to be a default program of neonatal CD4+ T-cells. Poor antibody production, affinity maturation, and germinal center reaction in vaccinated neonates are correlated with a limiting expansion of TFH lymphocytes. We review herein the factors accounting for and the implications of the unbalanced neonatal helper T-cell immunity.
Highlights
In comparison to adults, newborns display a heightened susceptibility to pathogens and a propensity to develop allergic diseases
Several works in mice first established that Th1-type responses could be induced in neonates with Th1-promoting inflammatory treatments, and brought some clues to explain the unbalanced Th1/Th2 neonatal immunity. This induction of Th1-cell development and, the modulation of the Th2-type response could be achieved by administration of IFN-γ itself [8], antigen-presenting cells (APCs)-derived IL-12 [9], dendritic cells (DCs) [10], live virus [11, 12], DNA vaccines [13], CpG nucleotides [14], or by CD40 triggering [15]
This could be a potential target to ensure neonatal protection to pathogens and to prevent development of allergic diseases, as neonatal Th17 immunity could compensate for the lack of Th1-type immune responses and oppose the Th2 pathway
Summary
Newborns display a heightened susceptibility to pathogens and a propensity to develop allergic diseases. At the level of APCs, in mice, the absence of IL-12p70 (composed of IL-12p35 and IL-12p40 chains) producing neonatal DCs in the first days of life favors the expression of the alternative receptor of IL-4 on neonatal Th1 cells, rending them sensitive to IL-4-induced apoptosis, and promotes Th2-cell development [21].
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