{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T05:11:36Z","timestamp":1788757896024,"version":"build-2803163510"},"reference-count":56,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Atopic dermatitis is a chronic inflammatory skin disease characterized by type 2 immune responses and severe itching; however, the molecular mechanisms linking lipid metabolism to epithelial\u2013immune signaling remain incompletely understood. Herein, we show that group IIF secreted phospholipase A\n                    <jats:sub>2<\/jats:sub>\n                    (PLA2G2F), which is induced by type 2 cytokines and selectively generates plasmalogen-derived lysophosphatidylethanolamine (lysoplasmalogen; P-LPE) in keratinocytes, contributes to the aggravation of atopic dermatitis and itching. Genetic deletion of\n                    <jats:italic>Pla2g2f<\/jats:italic>\n                    attenuated IL-33 expression in keratinocytes and reduced epidermal hyperplasia, serum IgE levels, type 2 inflammation and scratching behavior, without directly affecting neuronal structure and function, in a mouse model of atopic dermatitis. Topical application of a secreted PLA\n                    <jats:sub>2<\/jats:sub>\n                    inhibitor or forcible enzymatic degradation of P-LPE suppressed the itch response in wild-type mice, whereas exogenous P-LPE partially restored scratching behavior in\n                    <jats:italic>Pla2g2f<\/jats:italic>\n                    -deficient mice. Importantly, P-LPE levels were significantly elevated in the stratum corneum of patients with atopic dermatitis and positively correlated with disease severity. Collectively, the present study highlights that the PLA2G2F\/P-LPE axis, originally identified in psoriasis, is a key regulator that connects epidermal lipid metabolism to IL-33\u2013mediated type 2 inflammation and itching, suggesting that this pathway could be a novel therapeutic target and biomarker of this disease.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1880255","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T04:23:46Z","timestamp":1788755026000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["PLA2G2F\/lysoplasmalogen axis links epidermal lipid metabolism to type 2 inflammation and itch in atopic dermatitis"],"prefix":"10.3389","volume":"17","author":[{"given":"Yoshimi","family":"Miki","sequence":"first","affiliation":[{"name":"Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima 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