{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T15:10:37Z","timestamp":1791990637793,"version":"4.4.0"},"reference-count":88,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"112","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2025,10,24]]},"abstract":"<jats:p>\n                    A unique subpopulation of memory T helper 2 (T\n                    <jats:sub>H<\/jats:sub>\n                    2) cells expressing the interleukin-33 (IL-33) receptor ST2 drives allergic disease pathogenesis. However, the immunometabolic mechanisms that induce ST2\n                    <jats:sup>hi<\/jats:sup>\n                    memory T\n                    <jats:sub>H<\/jats:sub>\n                    2 cells remain unclear. We show using a mouse model of chronic allergic airway inflammation that long-chain unsaturated fatty acids (LC-UFAs) accumulate in the inflammatory milieu during chronic airway inflammation. Activated T\n                    <jats:sub>H<\/jats:sub>\n                    2 cells take up LC-UFAs, transiently store them in lipid droplets (LDs), and catabolize LDs through lipolysis and microlipophagy. LD catabolism regulated by adipose triglyceride lipase (ATGL) activates peroxisome proliferator\u2013activated receptor \u03b3 (PPAR\u03b3). PPAR\u03b3 then binds the\n                    <jats:italic toggle=\"yes\">Il1rl1<\/jats:italic>\n                    locus encoding ST2 and induces ST2\n                    <jats:sup>hi<\/jats:sup>\n                    effector and memory T\n                    <jats:sub>H<\/jats:sub>\n                    2 cells. In eosinophilic chronic rhinosinusitis, CD45RO\n                    <jats:sup>+<\/jats:sup>\n                    CD4 T cells in nasal polyps exhibit microlipophagy and an accessible\n                    <jats:italic toggle=\"yes\">IL1RL1<\/jats:italic>\n                    enhancer, indicating that these mechanisms are conserved in humans. Thus, the storage and catabolism of inflammatory milieu\u2013derived LC-UFAs direct pathogenic adaptive type 2 immunity, offering potential therapeutic strategies for persistent allergic inflammation.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.adp0849","type":"journal-article","created":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T17:58:09Z","timestamp":1761328689000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":7,"title":["Lipolysis-microlipophagy cascade regulated by adipose triglyceride lipase drives pathogenic adaptive type 2 immunity"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4336-9919","authenticated-orcid":true,"given":"Hiroyuki","family":"Yagyu","sequence":"first","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan."},{"name":"Department of Pulmonology, Graduate School of Medicine, 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