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- W2887624888 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." @default.
- W2887624888 created "2018-08-22" @default.
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- W2887624888 date "2018-08-17" @default.
- W2887624888 modified "2023-10-10" @default.
- W2887624888 title "Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy" @default.
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- W2887624888 doi "https://doi.org/10.1038/s41467-018-05608-4" @default.
- W2887624888 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6098117" @default.
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