{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T09:44:11Z","timestamp":1775123051382,"version":"3.50.1"},"reference-count":51,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,17]],"date-time":"2025-10-17T00:00:00Z","timestamp":1760659200000},"content-version":"vor","delay-in-days":16,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical &amp; Translational All"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Although IL\u201033\/ST2 signaling has been implicated in adult asthma, its contribution to early\u2010onset\u00a0allergic asthma remains poorly understood. Here, we examined the postnatal dynamics of IL\u201033 and its regulation by splenic ST2\n                      <jats:sup>+<\/jats:sup>\n                      erythroid progenitors (EPs).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Plasma IL\u201033 levels were measured in neonatal and young mice. Wild Type (WT) and\n                      <jats:italic>Il33<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice were exposed to house dust mite (HDM) to assess airway inflammation and asthma. ST2\n                      <jats:sup>+<\/jats:sup>\n                      EPs were analyzed for IL\u201033 responsiveness, transcriptomic\/epigenomic profiles, and IL\u201033 scavenging capacity. EP depletion was performed to evaluate their role in HDM\u2010induced inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Plasma IL\u201033 levels fluctuated during the postnatal period, peaking at postnatal day 7 (PND7). WT mice exhibited more severe HDM\u2010induced airway inflammation than\n                      <jats:italic>Il33<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. Splenic ST2\n                      <jats:sup>+<\/jats:sup>\n                      EPs, abundant in early life but absent by PND28, displayed minimal IL\u201033\u2013induced signaling or transcriptomic\/epigenomic alterations, yet efficiently scavenged IL\u201033. Depletion of EPs exacerbated HDM\u2010induced inflammation, accompanied by increased T follicular helper cells (Tfh) and IgE\n                      <jats:sup>+<\/jats:sup>\n                      B cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      ST2\n                      <jats:sup>+<\/jats:sup>\n                      EPs function as transient IL\u201033 scavengers during early life, attenuating its pro\u2010asthmatic effects and preserving immune homeostasis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/clt2.70111","type":"journal-article","created":{"date-parts":[[2025,10,18]],"date-time":"2025-10-18T03:23:36Z","timestamp":1760757816000},"source":"Crossref","is-referenced-by-count":1,"title":["ST2\n                    <sup>+<\/sup>\n                    Erythroid Progenitors Suppress Allergic Asthma by Scavenging IL\u201033 in Young Mice"],"prefix":"10.1002","volume":"15","author":[{"given":"Chang","family":"Li","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Key University Laboratory of Metabolism and Health of Guangdong, Joint Laboratory of Guangdong\u2010Hong Kong Universities for Vascular Homeostasis and Diseases, SUSTech Homeostatic Medicine Institute School of Medicine Southern University of Science and Technology  Shenzhen China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Key University Laboratory of Metabolism and Health of Guangdong, Joint Laboratory of Guangdong\u2010Hong Kong Universities for Vascular Homeostasis and Diseases, SUSTech Homeostatic Medicine Institute School of Medicine Southern University of Science and Technology  Shenzhen China"},{"name":"Flow Cytometry Core Facility Shenzhen Medical Academy of 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China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Key University Laboratory of Metabolism and Health of Guangdong, Joint Laboratory of Guangdong\u2010Hong Kong Universities for Vascular Homeostasis and Diseases, SUSTech Homeostatic Medicine Institute School of Medicine Southern University of Science and Technology  Shenzhen China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Heng","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Key University Laboratory of Metabolism and Health of Guangdong, Joint Laboratory of Guangdong\u2010Hong Kong Universities for Vascular Homeostasis and Diseases, SUSTech Homeostatic Medicine Institute School of Medicine Southern University of Science and Technology  Shenzhen China"},{"name":"Department of Oncology National Cancer Center\/National Clinical Research Center for 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