{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T20:17:26Z","timestamp":1792181846935,"version":"4.4.0"},"reference-count":73,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T00:00:00Z","timestamp":1622764800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T00:00:00Z","timestamp":1622764800000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T00:00:00Z","timestamp":1622764800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001961","name":"AXA Research Fund","doi-asserted-by":"publisher","award":["16-AXA-PDOC-078"],"award-info":[{"award-number":["16-AXA-PDOC-078"]}],"id":[{"id":"10.13039\/501100001961","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004328","name":"Genentech","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004328","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010663","name":"H2020 European Research Council","doi-asserted-by":"publisher","award":["742720"],"award-info":[{"award-number":["742720"]}],"id":[{"id":"10.13039\/100010663","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>\n                    Defective autophagy is strongly associated with chronic inflammation. Loss-of-function of the core autophagy gene\n                    <jats:italic>Atg16l1<\/jats:italic>\n                    increases risk for Crohn\u2019s disease in part by enhancing innate immunity through myeloid cells such as macrophages. However, autophagy is also recognized as a mechanism for clearance of certain intracellular pathogens. These divergent observations prompted a re-evaluation of ATG16L1 in innate antimicrobial immunity. In this study, we found that loss of\n                    <jats:italic>Atg16l1<\/jats:italic>\n                    in myeloid cells enhanced the killing of virulent\n                    <jats:italic>Shigella flexneri (S.flexneri)<\/jats:italic>\n                    , a clinically relevant enteric bacterium that resides within the cytosol by escaping from membrane-bound compartments. Quantitative multiplexed proteomics of murine bone marrow-derived macrophages revealed that ATG16L1 deficiency significantly upregulated proteins involved in the glutathione-mediated antioxidant response to compensate for elevated oxidative stress, which simultaneously promoted\n                    <jats:italic>S.flexneri<\/jats:italic>\n                    killing. Consistent with this, myeloid-specific deletion of\n                    <jats:italic>Atg16l1<\/jats:italic>\n                    in mice accelerated bacterial clearance in\n                    <jats:italic>vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Pharmacological induction of oxidative stress through suppression of cysteine import enhanced microbial clearance by macrophages. Conversely, antioxidant treatment of macrophages permitted\n                    <jats:italic>S.flexneri<\/jats:italic>\n                    proliferation. These findings demonstrate that control of oxidative stress by ATG16L1 and autophagy regulates antimicrobial immunity against intracellular pathogens.\n                  <\/jats:p>","DOI":"10.7554\/elife.62320","type":"journal-article","created":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T05:00:27Z","timestamp":1622782827000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.62320","source":"Crossref","is-referenced-by-count":16,"title":["Multiplexed proteomics of autophagy-deficient murine macrophages reveals enhanced antimicrobial immunity via the oxidative stress response"],"prefix":"10.7554","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9333-301X","authenticated-orcid":true,"given":"Timurs","family":"Maculins","sequence":"first","affiliation":[{"name":"Department of Cancer Immunology, Genentech, South San Francisco, United States"},{"name":"Institute of Biochemistry II, Goethe University, Frankfurt am Main, 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