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 () and Richard Saffery
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David Martino: The University of Melbourne
Melanie Neeland: The University of Melbourne
Thanh Dang: The University of Melbourne
Joanna Cobb: The University of Melbourne
Justine Ellis: The University of Melbourne
Alice Barnett: The University of Melbourne
Mimi Tang: The University of Melbourne
Peter Vuillermin: The University of Melbourne
Katrina Allen: The University of Melbourne
Richard Saffery: The University of Melbourne

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-05608-4

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