Zhang Li, Gianani Roberto, Nakayama Maki, Liu Edwin, Kobayashi Masakazu, Baschal Erin, Yu Liping, Babu Sunanda, Dawson Abby, Johnson Kelly, Jahromi Mohamed, Aly Theresa, Fain Pamela, Barker Jennifer, Rewers Marian, Eisenbarth George S
Barbara Davis Center for Childhood Diabetes, University of Colorado Denver Health Sciences Center, Aurora, CO 80010, USA.
Novartis Found Symp. 2008;292:85-94; discussion 94-8, 122-9, 202-3. doi: 10.1002/9780470697405.ch7.
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.
动物模型中的大量数据表明，1A型糖尿病是由T细胞介导的胰岛β细胞特异性破坏所致。有证据表明，在非肥胖糖尿病（NOD）小鼠模型中，胰岛素是主要自身抗原，特定的胰岛素肽B:9-23在发病机制中起核心作用。现在，结合遗传、免疫和代谢参数，也能够预测绝大多数个体1A型（免疫介导）糖尿病的发生。由于自身免疫的慢性性质以及疾病发生前β细胞功能的丧失，这种预测成为可能。鉴于能够预测1A型糖尿病，现在有可能在该疾病的各个阶段进行试验以预防β细胞破坏。
