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Immunity in the newborn is characterized by minimal Th1 function but an excess of Th2 activity. Since Th1 lymphocytes are important to counter microbes and Th2 cells favor allergies, the newborn faces susceptibility to microbial infections and allergic reactions. Delayed maturation of certain dendritic cells leads to limited IL-12 production during the neonatal period. The Th2 cytokine locus of neonatal CD4+ T cells is epigenetically poised for rapid and robust production of IL-4 and IL-13. Together, these circumstances lead to efficient differentiation of Th2 cells and the expression of an IL-4Rα/IL-13Rα1 heteroreceptor on Th1 cells. Upon rechallenge, Th2 cells rapidly produce IL-4 which utilizes the heteroreceptor to drive apoptosis of Th1 cells yielding the Th2 bias of neonatal immunity.

We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung infl ammation, which is a cardinal feature of asthma.

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