{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:22:18Z","timestamp":1790835738142,"version":"4.1.0"},"reference-count":88,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"735","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2024,2,21]]},"abstract":"<jats:p>Acute graft-versus-host disease (aGVHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation (allo-HCT), for which therapeutic options are limited. Strategies to promote intestinal tissue tolerance during aGVHD may improve patient outcomes. Using single-cell RNA sequencing, we identified a lipocalin-2 (LCN2)\u2013expressing neutrophil population in mice with intestinal aGVHD. Transfer of LCN2-overexpressing neutrophils or treatment with recombinant LCN2 reduced aGVHD severity, whereas the lack of epithelial or hematopoietic LCN2 enhanced aGVHD severity and caused microbiome alterations. Mechanistically, LCN2 induced insulin-like growth factor 1 receptor (IGF-1R) signaling in macrophages through the LCN2 receptor SLC22A17, which increased interleukin-10 (IL-10) production and reduced major histocompatibility complex class II (MHCII) expression. Transfer of LCN2-pretreated macrophages reduced aGVHD severity but did not reduce graft-versus-leukemia effects. Furthermore, LCN2 expression correlated with IL-10 expression in intestinal biopsies in multiple cohorts of patients with aGVHD, and LCN2 induced IGF-1R signaling in human macrophages. Collectively, we identified a LCN2-expressing intestinal neutrophil population that reduced aGVHD severity by decreasing MHCII expression and increasing IL-10 production in macrophages. This work provides the foundation for administration of LCN2 as a therapeutic approach for aGVHD.<\/jats:p>","DOI":"10.1126\/scitranslmed.adi1501","type":"journal-article","created":{"date-parts":[[2024,2,21]],"date-time":"2024-02-21T14:01:07Z","timestamp":1708524067000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":37,"title":["Lipocalin-2 expression identifies an intestinal regulatory neutrophil population during acute graft-versus-host disease"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-3763-7290","authenticated-orcid":true,"given":"Marie","family":"Czech","sequence":"first","affiliation":[{"name":"Department of Medicine I, Medical Center\u2013University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany."},{"name":"Faculty of Biology, University of Freiburg, 79104 Freiburg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0140-2750","authenticated-orcid":true,"given":"Sophia","family":"Schneider","sequence":"additional","affiliation":[{"name":"Department of Medicine I, Medical Center\u2013University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-0137-6378","authenticated-orcid":true,"given":"Nina","family":"Peltokangas","sequence":"additional","affiliation":[{"name":"Faculty of Biology, University of Freiburg, 79104 Freiburg, Germany."},{"name":"Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany."},{"name":"W\u00fcrzburg Institute of Systems Immunology, Max Planck Research Group at the Julius-Maximilians-Universit\u00e4t W\u00fcrzburg, 97078 W\u00fcrzburg, 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