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Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Exposure to fine particulate matter (PM\n                      <jats:sub>2.5<\/jats:sub>\n                      ) increases asthma severity and reduces glucocorticoid responsiveness in children, yet the molecular mechanisms underlying PM\n                      <jats:sub>2.5<\/jats:sub>\n                      sensitivity remain unclear. We previously identified a PM\n                      <jats:sub>2.5<\/jats:sub>\n                      -sensitive asthma phenotype and developed a PM\n                      <jats:sub>2.5<\/jats:sub>\n                      sensitivity polygenic risk score (sPRS) correlated with asthma exacerbations and lung function decline.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Research question<\/jats:title>\n                    <jats:p>\n                      We sought to determine whether genetic variants contributing to PM\n                      <jats:sub>2.5<\/jats:sub>\n                      sensitivity converge on specific biological pathways or transcriptional regulators, and whether children with a high sPRS exhibit immune transcriptional signatures consistent with heightened PM\n                      <jats:sub>2.5<\/jats:sub>\n                      susceptibility.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Genes implicated by sPRS variants were mapped using regulatory annotation tools and evaluated for pathway and transcription factor target enrichment. Peripheral blood mononuclear cells (PBMCs) from high- and low-sPRS children matched on long-term ambient PM\n                      <jats:sub>2.5<\/jats:sub>\n                      exposure were profiled using single-cell RNA sequencing. Donor-level pseudobulk differential expression was performed using a paired quasi-likelihood negative binomial framework, followed by exploratory pathway enrichment and perturbagen signature analyses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      sPRS-implicated genes were enriched for transcriptional regulators linked to SMAD2\/3- and MAPK-associated signaling, suggesting TGF-\u03b21-related pathway involvement. No genes reached false-discovery-rate-adjusted significance at the donor level in this small, matched cohort. However, secondary pathway-level analyses demonstrated concordant enrichment across multiple immune populations in inflammatory and stress-response signaling programs previously linked to PM\n                      <jats:sub>2.5<\/jats:sub>\n                      exposure. Perturbagen signature analyses likewise highlighted small-molecule regulators of TGF-\u03b21-associated pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>\n                      These integrative genomic and transcriptomic analyses nominate TGF-\u03b21-SMAD\/MAPK signaling as a biologically plausible axis of genetic susceptibility to PM\n                      <jats:sub>2.5<\/jats:sub>\n                      in pediatric asthma. Given the modest sample size and indirect nature of enrichment-based inference, these findings should be considered hypothesis-generating and motivate targeted functional validation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1644537","type":"journal-article","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T05:21:50Z","timestamp":1770096110000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Genetic susceptibility to PM2.5 exposure and transcriptional responses in pediatric asthma: insights from single-cell transcriptomics"],"prefix":"10.3389","volume":"17","author":[{"given":"Jelte","family":"Kelchtermans","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]},{"name":"Perelman School of Medicine, University of Pennsylvania","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huiqi","family":"Qu","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cuiping","family":"Hou","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Mentch","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon A.","family":"McGrath-Morrow","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]},{"name":"Perelman School of Medicine, University of Pennsylvania","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hakon","family":"Hakonarson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Philadelphia","place":["Philadelphia, PA, United States"]},{"name":"Perelman School of Medicine, University of Pennsylvania","place":["Philadelphia, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,2,3]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.oneear.2024.09.022","article-title":"Long-term exposure to PM2.5 has significant adverse effects on childhood and adult asthma: A global meta-analysis and health impact assessment","volume":"7","author":"Ni","year":"2024","journal-title":"One Earth"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s11356-015-5321-x","article-title":"The impact of PM2.5 on asthma emergency department visits: a systematic review and meta-analysis","volume":"23","author":"Fan","year":"2016","journal-title":"Environ Sci pollut Res"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1016\/j.jaci.2017.05.010","article-title":"Environmental determinants of allergy and asthma in early life","volume":"140","author":"Burbank","year":"2017","journal-title":"J Allergy Clin Immunol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.envres.2017.08.038","article-title":"The impact of prenatal exposure to air pollution on childhood wheezing and asthma: A systematic review","volume":"159","author":"Hehua","year":"2017","journal-title":"Environ Res"},{"key":"B5","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1016\/j.envint.2016.11.012","article-title":"Exposure to traffic-related air pollution and risk of development of childhood asthma: A systematic review and meta-analysis","volume":"100","author":"Khreis","year":"2017","journal-title":"Environ Int"},{"key":"B6","volume-title":"GINA MAIN REPORT","year":"2024"},{"key":"B7","doi-asserted-by":"publisher","first-page":"48","DOI":"10.1016\/j.scitotenv.2012.11.070","article-title":"Air pollution and respiratory symptoms among children with asthma: vulnerability by corticosteroid use and residence area","volume":"448","author":"Lewis","year":"2013","journal-title":"Sci Total Environ"},{"key":"B8","volume-title":"State of global air 2024. 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