<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Suen JL</submitter><funding>Ministry of Science and Technology</funding><funding>Shenzhen Peacock Plan</funding><funding>Kaohsiung Medical University</funding><funding>Center of Excellence for Environmental Medicine, Kaohsiung Medical University</funding><funding>National Health Research Institutes</funding><funding>NCI NIH HHS</funding><funding>HSRD VA</funding><pagination>603831</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7786300</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><pubmed_abstract>The developmental origin of allergic diseases has been suggested, but the molecular basis remains enigmatic. Exposure to environmental factors, such as di-(2-ethylhexyl) phthalate (DEHP; a common plasticizer), is suggested to be associated with increased childhood allergic asthma, but the causal relationship and its underlying mechanism remain unknown. This study explored the transgenerational mechanism of DEHP on allergic asthma and dendritic cell (DC) homeostasis through epigenetic modification. In a murine model, ancestral exposure of C57BL/6 mice to low-dose DEHP led to trans-generational promoter hypomethylation of the &lt;i>insulin-like growth factor 2 receptor&lt;/i> (&lt;i>Igf2r&lt;/i>), concomitant with enhanced Igf2r expression and increased apoptosis prominently in CD8α&lt;sup>+&lt;/sup> DCs upon</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Environmental Factor-Mediated Transgenerational Inheritance of &lt;i>Igf2r&lt;/i> Hypomethylation and Pulmonary Allergic Response &lt;i>via&lt;/i> Targeting Dendritic Cells.</pubmed_title><pmcid>PMC7786300</pmcid><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>R50 CA211524</funding_grant_id><funding_grant_id>CDA 10-014</funding_grant_id><funding_grant_id>MOST 105-2320-B-037-015, MOST 106-2314-B-037-072, MOST 107-2314-B-037-003, MOST 108-2314-B-037-001, MOST 108-2320-B-037-010</funding_grant_id><funding_grant_id>The Talent Plan (105KMUOR04), KMU-TC108A01</funding_grant_id><funding_grant_id>KMU-TP104A05, KMU-TP105A02</funding_grant_id><funding_grant_id>NHRI-102A1-PDCO-03010201, EOPP10-014, EOSP07-014</funding_grant_id><pubmed_authors>Wang CJ</pubmed_authors><pubmed_authors>Kuo FC</pubmed_authors><pubmed_authors>Li YH</pubmed_authors><pubmed_authors>Lee CL</pubmed_authors><pubmed_authors>Tran M</pubmed_authors><pubmed_authors>Yan PS</pubmed_authors><pubmed_authors>Wu MT</pubmed_authors><pubmed_authors>Suen JL</pubmed_authors><pubmed_authors>Wu CF</pubmed_authors><pubmed_authors>Hung CH</pubmed_authors><pubmed_authors>Huang SK</pubmed_authors><pubmed_authors>Chan MWY</pubmed_authors><pubmed_authors>Wu TT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Environmental Factor-Mediated Transgenerational Inheritance of &lt;i>Igf2r&lt;/i> Hypomethylation and Pulmonary Allergic Response &lt;i>via&lt;/i> Targeting Dendritic Cells.</name><description>The developmental origin of allergic diseases has been suggested, but the molecular basis remains enigmatic. Exposure to environmental factors, such as di-(2-ethylhexyl) phthalate (DEHP; a common plasticizer), is suggested to be associated with increased childhood allergic asthma, but the causal relationship and its underlying mechanism remain unknown. This study explored the transgenerational mechanism of DEHP on allergic asthma and dendritic cell (DC) homeostasis through epigenetic modification. In a murine model, ancestral exposure of C57BL/6 mice to low-dose DEHP led to trans-generational promoter hypomethylation of the &lt;i>insulin-like growth factor 2 receptor&lt;/i> (&lt;i>Igf2r&lt;/i>), concomitant with enhanced Igf2r expression and increased apoptosis prominently in CD8α&lt;sup>+&lt;/sup> DCs upon</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2026-05-02T06:36:11.703Z</modification><creation>2025-04-04T07:16:30.403Z</creation></dates><accession>S-EPMC7786300</accession><cross_references><pubmed>33424850</pubmed><doi>10.3389/fimmu.2020.603831</doi></cross_references></HashMap>