{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:57:59Z","timestamp":1790506679526,"version":"4.1.0"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2022,2,1]],"date-time":"2022-02-01T00:00:00Z","timestamp":1643673600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["VO944\/9-1 and CRC1181_A02"],"award-info":[{"award-number":["VO944\/9-1 and CRC1181_A02"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["U19 AI136443"],"award-info":[{"award-number":["U19 AI136443"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Eosinophils are potent innate effector cells associated mainly with type 2 immune responses elicited by helminths and allergens. Their activity needs to be tightly controlled to prevent severe inflammation and tissue damage. Eosinophil degranulation and secretion of inflammatory effector molecules, including cytokines, chemokines, and lipid mediators, can be regulated by activating and inhibitory receptors on the cell surface. In this study, we investigated the modulation of proliferation, apoptosis, gene expression, and cytokine\/chemokine secretion from IL-33\u2013activated Mus musculus eosinophils on cross-linking of the transmembrane receptor Sialic acid\u2013binding Ig-like lectin F (Siglec-F). Siglec-F contains an ITIM plus an ITIM-like motif in its intracellular tail and is mainly regarded as an inhibitory and apoptosis-inducing receptor. In vitro costimulation of bone marrow\u2013derived eosinophils with anti\u2013Siglec-F and IL-33 compared with treatment with either alone led to enhanced STAT6 phosphorylation, stronger induction of hypoxia\/glycolysis-related proinflammatory genes, and elevated secretion of type 2 cytokines (IL-4, IL-13) and chemokines (CCL3, CCL4) with only minor effects on proliferation and apoptosis. Using a competitive mixed bone marrow chimera approach with wild-type and Siglec-F\u2013deficient eosinophils, we observed no evidence for Siglec-F\u2013regulated inhibition of Aspergillus fumigatus\u2013elicited lung eosinophilia. Truncation of the Siglec-F cytoplasmic tail, but not mutation of the ITIM and ITIM-like motifs, ablated the effect of enhanced cytokine\/chemokine secretion. This provides evidence for an ITIM phosphorylation-independent signaling pathway from the cytoplasmic tail of the Siglec-F receptor that enhances effector molecule release from activated eosinophils.<\/jats:p>","DOI":"10.4049\/jimmunol.2100184","type":"journal-article","created":{"date-parts":[[2022,1,7]],"date-time":"2022-01-07T17:05:34Z","timestamp":1641575134000},"page":"732-744","source":"Crossref","is-referenced-by-count":16,"title":["Siglec-F Promotes IL-33\u2013Induced Cytokine Release from Bone Marrow\u2013Derived Eosinophils Independently of the ITIM and ITIM-like Motif Phosphorylation"],"prefix":"10.1093","volume":"208","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4977-0009","authenticated-orcid":false,"given":"Stefanie","family":"Westermann","sequence":"first","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0598-9714","authenticated-orcid":false,"given":"Axel","family":"Dietschmann","sequence":"additional","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Doehler","sequence":"additional","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirstin","family":"Castiglione","sequence":"additional","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9411-6009","authenticated-orcid":false,"given":"Bruce S","family":"Bochner","sequence":"additional","affiliation":[{"name":"Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine , Chicago, IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6650-0639","authenticated-orcid":false,"given":"David","family":"Voehringer","sequence":"additional","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3241-4542","authenticated-orcid":false,"given":"Daniel","family":"Radtke","sequence":"additional","affiliation":[{"name":"Department of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg , Erlangen,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2022,2,1]]},"reference":[{"key":"2025021008530964700_r1","doi-asserted-by":"crossref","first-page":"1125","DOI":"10.1093\/glycob\/cwi097","article-title":"Mouse Siglec-F and human Siglec-8 are functionally convergent paralogs that are selectively expressed on eosinophils and recognize 6\u2032-sulfo-sialyl Lewis X as a preferred glycan ligand","volume":"15","author":"Tateno","year":"2005","journal-title":"Glycobiology"},{"key":"2025021008530964700_r2","doi-asserted-by":"crossref","first-page":"45128","DOI":"10.1074\/jbc.M108573200","article-title":"Cloning and characterization of a novel mouse Siglec, mSiglec-F: differential evolution of the mouse and human (CD33) Siglec-3-related gene clusters","volume":"276","author":"Angata","year":"2001","journal-title":"J. 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Immunol."},{"key":"2025021008530964700_r4","doi-asserted-by":"crossref","first-page":"4280","DOI":"10.1182\/blood-2006-08-039255","article-title":"Defining the in vivo function of Siglec-F, a CD33-related Siglec expressed on mouse eosinophils","volume":"109","author":"Zhang","year":"2007","journal-title":"Blood"},{"key":"2025021008530964700_r5","doi-asserted-by":"crossref","first-page":"5014","DOI":"10.1182\/blood-2002-10-3058","article-title":"Ligation of Siglec-8: a selective mechanism for induction of human eosinophil apoptosis","volume":"101","author":"Nutku","year":"2003","journal-title":"Blood"},{"key":"2025021008530964700_r6","doi-asserted-by":"crossref","first-page":"1156","DOI":"10.1111\/j.1398-9995.2008.01709.x","article-title":"Siglec-F antibody administration to mice selectively reduces blood and tissue eosinophils","volume":"63","author":"Zimmermann","year":"2008","journal-title":"Allergy"},{"key":"2025021008530964700_r7","doi-asserted-by":"crossref","first-page":"43","DOI":"10.1002\/JLB.3HI0120-381R","article-title":"Frontline science: superior mouse eosinophil depletion in vivo targeting transgenic Siglec-8 instead of endogenous Siglec-F: mechanisms and pitfalls","volume":"108","author":"Knuplez","year":"2020","journal-title":"J. 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