{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:50:04Z","timestamp":1790747404547,"version":"4.1.0"},"reference-count":26,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,8,7]],"date-time":"2017-08-07T00:00:00Z","timestamp":1502064000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001711","name":"Schweizerischer Nationalfonds zur F\u00f6rderung der Wissenschaftlichen Forschung","doi-asserted-by":"publisher","award":["31003A_173215"],"award-info":[{"award-number":["31003A_173215"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001711","name":"Schweizerischer Nationalfonds zur F\u00f6rderung der Wissenschaftlichen Forschung","doi-asserted-by":"publisher","award":["310030_166473"],"award-info":[{"award-number":["310030_166473"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The importance of extracellular traps (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>s) in innate immunity is well established, but the molecular mechanisms responsible for their formation remain unclear and in scientific dispute. <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>s have been defined as extracellular <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> scaffolds associated with the granule proteins of eosinophils or neutrophils. They are capable of killing bacteria extracellularly. Based mainly on results with phosphoinositide 3\u2010kinase (<jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3K) inhibitors such as 3\u2010methyladenine (3\u2010<jats:styled-content style=\"fixed-case\">MA<\/jats:styled-content>) and wortmannin, which are commonly used to inhibit autophagy, several groups have reported that autophagy is required for neutrophil extracellular trap (<jats:styled-content style=\"fixed-case\">NET<\/jats:styled-content>) formation. We decided to investigate this apparent dependence on autophagy for <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> release and generated genetically modified mice that lack, specifically in eosinophils or neutrophils, <jats:italic>autophagy\u2010related 5<\/jats:italic> (<jats:italic>Atg5<\/jats:italic>), a gene encoding a protein essential for autophagosome formation. Interestingly, neither eosinophils nor neutrophils from <jats:italic>Atg5<\/jats:italic>\u2010deficient mice exhibited abnormalities in <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> formation upon physiological activation or exposure to low concentrations of <jats:styled-content style=\"fixed-case\">PMA<\/jats:styled-content>, although we could confirm that human and mouse eosinophils and neutrophils, after pre\u2010treatment with inhibitors of class <jats:styled-content style=\"fixed-case\">III PI<\/jats:styled-content>3K, show a block both in reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) production and in <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> formation. The so\u2010called late autophagy inhibitors bafilomycin A1 and chloroquine, on the other hand, were without effect. These data indicate that <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> formation occurs independently of autophagy and that the inhibition of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production and <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> formation in the presence of 3\u2010<jats:styled-content style=\"fixed-case\">MA<\/jats:styled-content> and wortmannin is probably owing to their additional ability to block the class I <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3Ks, which are involved in signalling cascades initiated by triggers of <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content> formation.<\/jats:p>","DOI":"10.1111\/imm.12790","type":"journal-article","created":{"date-parts":[[2017,7,13]],"date-time":"2017-07-13T11:40:36Z","timestamp":1499946036000},"page":"517-525","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":93,"title":["Neither eosinophils nor neutrophils require <scp>ATG<\/scp>5\u2010dependent autophagy for extracellular <scp>DNA<\/scp> trap formation"],"prefix":"10.1111","volume":"152","author":[{"given":"Nina","family":"Germic","sequence":"first","affiliation":[{"name":"Institute of Pharmacology University of Bern Bern Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darko","family":"Stojkov","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology University of Bern Bern Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin","family":"Oberson","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology 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