{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T07:06:11Z","timestamp":1790233571210,"version":"4.1.0"},"reference-count":19,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T00:00:00Z","timestamp":1773878400000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K08AR081405"],"award-info":[{"award-number":["K08AR081405"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P01HL174442"],"award-info":[{"award-number":["P01HL174442"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["UL1TR002243"],"award-info":[{"award-number":["UL1TR002243"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["IK2BX005376"],"award-info":[{"award-number":["IK2BX005376"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["ACR Open Rheumatology"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Systemic lupus erythematosus (SLE) is an autoimmune disease that affects numerous organs. Neutrophil extracellular traps (NETs) contribute to sterile inflammation and autoantibody generation in SLE. Isolevuglandins (isoLGs) are reactive oxygen species that are formed during NETosis and contribute to chromatin expansion. Scavenging of isoLGs attenuates SLE disease activity and hypertension in murine models of SLE. We hypothesized that isoLGs drive NETosis in SLE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Neutrophils were isolated from patients with SLE (n\u00a0=\u00a06), treated with the isoLG scavenger ethyl\u20102\u2010hydroxybenzylamine (Et\u20102\u2010HOBA), and evaluated for NETosis by immunofluorescence. Single\u2010cell sequencing was performed on lymphoid tissue from SLE\u2010prone\n                      <jats:italic>B6.SLE123<\/jats:italic>\n                      mice treated with the isoLG scavenger 2\u2010hydroxybenzylamine (2\u2010HOBA). Flow cytometry was performed to quantify neutrophils and NETs in\n                      <jats:italic>B6.SLE123<\/jats:italic>\n                      mice (n\u00a0=\u00a011\u201315).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In neutrophils isolated from patients with SLE, Et\u20102\u2010HOBA prevented NETosis (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.05). In SLE\u2010prone mice, 2\u2010HOBA reduced neutrophil counts, inflammatory gene expression, circulating neutrophil counts (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001), and aortic NETosis (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest that isoLGs contribute to systemic autoimmunity and vascular inflammation by driving neutrophil migration and NETosis in SLE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acr2.90015","type":"journal-article","created":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T07:57:10Z","timestamp":1773907030000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Scavenging of Isolevuglandins Attenuates Neutrophil Migration and Neutrophil Extracellular Trap Formation in Systemic Lupus Erythematosus"],"prefix":"10.1002","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9752-4219","authenticated-orcid":false,"given":"Jaya","family":"Krishnan","sequence":"first","affiliation":[{"name":"Division of Clinical Pharmacology, Department of Medicine Vanderbilt University Medical Center  Nashville Tennessee"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N\u00e9stor","family":"de la Visitaci\u00f3n","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Department of Medicine Vanderbilt University Medical Center  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