Li Zhang, Roberto Gianani, Maki Nakayama, Edwin Liu, Masakazu Kobayashi, Erin Baschal, Liping Yu, Sunanda Babu, Abby Dawson, Kelly Johnson, Mohamed Jahromi, Theresa Aly, Pamela Fain, Jennifer Barker, Marian Rewers, George S Eisenbarth
{"title":"Type 1 diabetes: chronic progressive autoimmune disease.","authors":"Li Zhang, Roberto Gianani, Maki Nakayama, Edwin Liu, Masakazu Kobayashi, Erin Baschal, Liping Yu, Sunanda Babu, Abby Dawson, Kelly Johnson, Mohamed Jahromi, Theresa Aly, Pamela Fain, Jennifer Barker, Marian Rewers, George S Eisenbarth","doi":"10.1002/9780470697405.ch7","DOIUrl":null,"url":null,"abstract":"<p><p>A wealth of data in animal models indicates that type 1A diabetes results from T cell-mediated specific destruction of islet beta cells. There is evidence for the NOD mouse model that insulin is the primary autoantigen and a specific insulin peptide B:9-23 is central to pathogenesis. It is also now possible to predict the development of type 1A (immune mediated) diabetes for the great majority of individuals with a combination of genetic, immunological and metabolic parameters. Such prediction is possible because of the chronic nature of the autoimmunity and loss of beta cell function that precedes the disease. Given the ability to predict type 1A diabetes trials at all stages of the disorder to prevent beta cell destruction are now possible.</p>","PeriodicalId":19323,"journal":{"name":"Novartis Foundation Symposium","volume":"292 ","pages":"85-94; discussion 94-8, 122-9, 202-3"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/9780470697405.ch7","citationCount":"32","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Novartis Foundation Symposium","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/9780470697405.ch7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 32
Abstract
A wealth of data in animal models indicates that type 1A diabetes results from T cell-mediated specific destruction of islet beta cells. There is evidence for the NOD mouse model that insulin is the primary autoantigen and a specific insulin peptide B:9-23 is central to pathogenesis. It is also now possible to predict the development of type 1A (immune mediated) diabetes for the great majority of individuals with a combination of genetic, immunological and metabolic parameters. Such prediction is possible because of the chronic nature of the autoimmunity and loss of beta cell function that precedes the disease. Given the ability to predict type 1A diabetes trials at all stages of the disorder to prevent beta cell destruction are now possible.