{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:28:18Z","timestamp":1761676098170},"reference-count":0,"publisher":"American Diabetes Association","issue":"7","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1995,7,1]]},"abstract":"<jats:p>Transgenic mice that express mouse B7-1 (mB7-1, recently designated CD80) on their pancreatic \u03b2-cells maintain normal islet architecture, have normal pancreatic insulin content, and only rarely spontaneously develop insulitis and diabetes. Nevertheless, these mice display an extreme sensitivity to streptozotocin (STZ)-induced diabetes. Female mice were administered two STZ doses intraperitoneally, 20 and 40 mg\/kg body wt, each for five consecutive days. Nontransgenic but otherwise syngeneic mice responded to the STZ with a moderate diminution in pancreatic insulin content but not with persistent glycosuria. In striking contrast, STZ administered to transgenic mice resulted in a severe diminution of pancreatic insulin content and in diabetes. Notably, the lower STZ dose resulted in diabetes only after a prolonged (26- to 100-day) latency. STZ-induced diabetes appears to be T-cell dependent, since treatment with T-cell\u2013depleting (and in particular CD8+ subset-depleting) antibodies ameliorated the response. Anti-mB7-1 monoclonal antibody administration also prevented STZ-induced diabetes. Thus, unmasked mB7-1 is a required component in the pathway resulting in \u03b2-cell killing. Immunohistological analysis revealed that early after STZ administration, both mB7-1 transgenic and nontransgenic mice developed insulitis. While this insulitis resolved in the nontransgenic mice, the islet-infiltrating CD4+ and CD8+ T-cells in the transgenic mice were associated with complete \u03b2-cell destruction. These data suggest that STZ-induced diabetes in mB7-1 transgenic mice is an immune-mediated process with distinct potential advantages over existing insulindependent diabetes models.<\/jats:p>","DOI":"10.2337\/diab.44.7.816","type":"journal-article","created":{"date-parts":[[2013,9,19]],"date-time":"2013-09-19T17:22:06Z","timestamp":1379611326000},"page":"816-823","update-policy":"http:\/\/dx.doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":21,"title":["Very-Low-Dose Streptozotocin Induces Diabetes in Insulin Promoter-mB7-1 Transgenic Mice"],"prefix":"10.2337","volume":"44","author":[{"given":"David M","family":"Harlan","sequence":"first","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michelle A","family":"Barnett","sequence":"additional","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryo","family":"Abe","sequence":"additional","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Klaus","family":"Pechhold","sequence":"additional","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noelle B","family":"Patterson","sequence":"additional","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gary S","family":"Gray","sequence":"additional","affiliation":[{"name":"Repligen Corporation\u2008Cambridge, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carl H","family":"June","sequence":"additional","affiliation":[{"name":"Immune Cell Biology Program, Naval Medical Research Institute\u2008Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","container-title":["Diabetes"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.org\/diabetes\/diabetes\/article-pdf\/44\/7\/816\/337737\/44-7-816.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article-pdf\/44\/7\/816\/337737\/44-7-816.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T16:28:13Z","timestamp":1667406493000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article\/44\/7\/816\/10387\/Very-Low-Dose-Streptozotocin-Induces-Diabetes-in"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,7,1]]},"references-count":0,"journal-issue":{"issue":"7","published-print":{"date-parts":[[1995,7,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diab.44.7.816","relation":{},"ISSN":["0012-1797","1939-327X"],"issn-type":[{"value":"0012-1797","type":"print"},{"value":"1939-327X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,7,1]]}}}