{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T17:06:29Z","timestamp":1781802389206,"version":"3.54.5"},"reference-count":51,"publisher":"American Diabetes Association","issue":"1","license":[{"start":{"date-parts":[[2016,12,20]],"date-time":"2016-12-20T00:00:00Z","timestamp":1482192000000},"content-version":"vor","delay-in-days":55,"URL":"http:\/\/www.diabetesjournals.org\/content\/license"}],"funder":[{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:p>Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing \u03b2-cells in the pancreas. Thereby, the chemokine CXC-motif ligand 10 (CXCL10) plays an important role in the recruitment of autoaggressive lymphocytes to the islets of Langerhans. Transplantation of isolated islets as a promising therapy for T1D has been hampered by early graft rejection. Here, we investigated the influence of CXCL10 on the autoimmune destruction of islet isografts using RIP-LCMV mice expressing a lymphocytic choriomeningitis virus (LCMV) protein in the \u03b2-cells. RIP-LCMV islets express CXCL10 after isolation and maintain CXCL10 production after engraftment. Thus, we isolated islets from either normal or CXCL10-deficient RIP-LCMV mice and transferred them under the kidney capsule of diabetic RIP-LCMV mice. We found that the autoimmune destruction of CXCL10-deficient islet isografts was significantly reduced. The autoimmune destruction was also diminished in mice administered with an anti-CXCL10 antibody. The persistent protection from autoimmune destruction was paralleled by an increase in FoxP3+ regulatory T cells within the cellular infiltrates around the islet isografts. Consequently, CXCL10 might influence the cellular composition locally in the islet graft, thereby playing a role in the autoimmune destruction. CXCL10 might therefore constitute a potential therapeutic target to prolong islet graft survival.<\/jats:p>","DOI":"10.2337\/db16-0547","type":"journal-article","created":{"date-parts":[[2016,10,27]],"date-time":"2016-10-27T02:49:50Z","timestamp":1477536590000},"page":"113-126","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":33,"title":["Islet-Expressed CXCL10 Promotes Autoimmune Destruction of Islet Isografts in Mice With Type 1 Diabetes"],"prefix":"10.2337","volume":"66","author":[{"given":"Christine","family":"Bender","sequence":"first","affiliation":[{"name":"Institute for Pharmacology and Toxicology, Pharmazentrum Frankfurt\/Center for Drug Research, Development, and Safety (ZAFES), Goethe University Hospital Frankfurt, Frankfurt am Main, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Selina","family":"Christen","sequence":"additional","affiliation":[{"name":"Institute for Pharmacology and 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