{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T21:19:26Z","timestamp":1761513566124,"version":"3.38.0"},"reference-count":61,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2015,2,1]],"date-time":"2015-02-01T00:00:00Z","timestamp":1422748800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>In multiple clinical conditions, including trauma and hemorrhage, reperfusion magnifies ischemic tissue damage. Ischemia induces expression of multiple neoantigens, including lipid alterations that are recognized by the serum protein, \u03b22-glycoprotein I (\u03b22-GPI). During reperfusion, binding of \u03b22-GPI by naturally occurring Abs results in an excessive inflammatory response that may lead to death. As \u03b22-GPI is critical for intestinal ischemia\/reperfusion (IR)-induced tissue damage and TLR2 is one of the proposed receptors for \u03b22-GPI, we hypothesized that IR-induced intestinal damage and inflammation require TLR2. Using TLR2\u2212\/\u2212 mice, we demonstrate that TLR2 is required for IR-induced mucosal damage, as well as complement activation and proinflammatory cytokine production. In response to IR, TLR2\u2212\/\u2212 mice have increased serum \u03b22-GPI compared with wild-type mice, but \u03b22-GPI is not deposited on ischemic intestinal tissue. In addition, TLR2\u2212\/\u2212 mice also did not express other novel Ags, suggesting a sequential response. Unlike other TLRs, TLR2\u2212\/\u2212 mice lacked the appropriate Ab repertoire to induce intestinal IR tissue damage or inflammation. Together, these data suggest that, in addition to the inflammatory response, IR-induced injury requires TLR2 for naturally occurring Ab production.<\/jats:p>","DOI":"10.4049\/jimmunol.1303124","type":"journal-article","created":{"date-parts":[[2014,12,25]],"date-time":"2014-12-25T05:57:06Z","timestamp":1419487026000},"page":"1190-1198","source":"Crossref","is-referenced-by-count":16,"title":["TLR2 Modulates Antibodies Required for Intestinal Ischemia\/Reperfusion-Induced Damage and Inflammation"],"prefix":"10.1093","volume":"194","author":[{"given":"Michael R","family":"Pope","sequence":"first","affiliation":[{"name":"Division of Biology, Kansas State University , Manhattan, KS 66506"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sherry D","family":"Fleming","sequence":"additional","affiliation":[{"name":"Division of Biology, Kansas State University , Manhattan, KS 66506"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2015,2,1]]},"reference":[{"key":"2025030704570238500_r1","doi-asserted-by":"crossref","first-page":"76","DOI":"10.9738\/CC112.1","article-title":"Risk factors affecting mortality in acute mesenteric ischemia and mortality rates: a single center experience","volume":"98","author":"Aliosmanoglu","year":"2013","journal-title":"Int. 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