Zhang et al. report altered immunity at birth (based on analyzing cord blood immune cell components and cytokine secretion) in kids that later develop food allergies., and skewing towards a Th2 phenotype. These findings are surprising to me- I would guess that these changes would be more related to postnatal exposures and microbiome makeup… I’d also be curious to know correlation with mom’s allergy and/or medication history.
Sci Transl Med. 2016 Jan 13;8(321):321ra8. doi: 10.1126/scitranslmed.aad4322.
Cord blood monocyte-derived inflammatory cytokines suppress IL-2 and induce nonclassic “TH2-type” immunity associated with development of food allergy.
Zhang Y1, Collier F2, Naselli G3, Saffery R4, Tang ML4, Allen KJ4, Ponsonby AL4, Harrison LC5, Vuillermin P6; BIS Investigator Group.
Abstract
Food allergy is a major health burden in early childhood. Infants who develop food allergy display a proinflammatory immune profile in cord blood, but how this is related to interleukin-4 (IL-4)/T helper 2 (TH2)-type immunity characteristic of allergy is unknown. In a general population-derived birth cohort, we found that in infants who developed food allergy, cord blood displayed a higher monocyte to CD4(+) T cell ratio and a lower proportion of natural regulatory T cell (nTreg) in relation to duration of labor. CD14(+) monocytes of food-allergic infants secreted higher amounts of inflammatory cytokines (IL-1β, IL-6, and tumor necrosis factor-α) in response to lipopolysaccharide. In the presence of the mucosal cytokine transforming growth factor-β, these inflammatory cytokines suppressed IL-2 expression by CD4(+) T cells. In the absence of IL-2, inflammatory cytokines decreased the number of activated nTreg and diverted the differentiation of both nTreg and naïve CD4(+) T cells toward an IL-4-expressing nonclassical TH2 phenotype. These findings provide a mechanistic explanation for susceptibility to food allergy in infants and suggest anti-inflammatory approaches to its prevention.
PMID: 26764159 [PubMed – in process]