Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy

David Martino, Melanie Neeland, Thanh Dang, Joanna Cobb, Justine Ellis, Alice Barnett, Mimi Tang, Peter Vuillermin, Katrina Allen, Richard Saffery

Research output: Contribution to journalArticlepeer-review

49 Citations (Scopus)


Food allergy poses a significant clinical and public health burden affecting 2–10% of infants. Using integrated DNA methylation and transcriptomic profiling, we found that polyclonal activation of naive CD4+ T cells through the T cell receptor results in poorer lymphoproliferative responses in children with immunoglobulin E (IgE)-mediated food allergy. Reduced expression of cell cycle-related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) underpins this suboptimal response. Infants who fail to resolve food allergy in later childhood exhibit cumulative increases in epigenetic disruption at T cell activation genes and poorer lymphoproliferative responses compared to children who resolved food allergy. Our data indicate epigenetic dysregulation in the early stages of signal transduction through the T cell receptor complex, and likely reflects pathways modified by gene–environment interactions in food allergy.

Original languageEnglish
Article number3308
JournalNature Communications
Issue number1
Publication statusPublished - 1 Dec 2018


Dive into the research topics of 'Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy'. Together they form a unique fingerprint.

Cite this