Genome-wide gene expression profiling reveals that CD274 is up-regulated new-onset type 1 diabetes mellitus
Genome-wide gene expression profiling reveals that CD274 is up-regulated new-onset type 1 diabetes mellitus
复制标题
全基因组基因表达谱揭示 CD274 在新发 1 型糖尿病中表达上调
DOI：
10.1007/s00592-017-1005-y
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发表时间：
2017-08-01
影响因子：
3.8
通讯作者：
Hu, Ji
中科院分区：
文献类型：
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作者：
Fang, Chen;Huang, Yun;Hu, Ji
早期研究已经确定1型糖尿病（T1 DM）是由产生胰岛素的胰腺β细胞的自身免疫破坏引起的疾病。T1 DM的遗传、环境和免疫发病机制是T1 DM研究的三大支柱。本研究试图了解T1 DM发病过程中基因表达谱的变化。结果对不同GEO数据集进行综合分析，并比较T1 DM发病时或发病前T1 DM样本中基因表达水平的结果，在T1 DM发病前1年和T1 DM发病时的胰岛自身抗体显示，编码PD-L1的CD 274在新发T1 DM样本中上调。CD 274在正常对照组中的表达水平较稳定，但在自身抗体产生后至T1 DM发病时表达水平逐渐上调。结论CD 274在T1 DM患者中的表达上调可能与T1 DM的发病有关。PD-L1可能在防止胰岛自身免疫性破坏中发挥保护作用，这可能有助于研究人员找到防止T1 DM胰腺β细胞破坏过程的策略。
Aims Early studies have identified type 1 diabetes mellitus (T1DM) as a disease that is caused by the autoimmune destruction of the insulin-producing pancreatic beta-cells. Genetics, environment and the immune pathogenesis of T1DM are three major pillars of T1DM research. We try to understand the changes in the gene expression profile during the pathogenesis of T1DM.Methods We performed a systematic search in the Gene Expression Omnibus (GEO) database for microarray studies of T1DM with samples taken at or before the T1DM onset.Results The results of an integrated analysis of different GEO datasets and a comparison of the gene expression level in T1DM samples taken at the time of appearance of the islet autoantibodies, 1 year before T1DM onset, and at the time of T1DM onset showed that CD274, which encodes PD-L1, was up-regulated in the newly onset T1DM samples. CD274 had a stable expression level in the control samples but showed a gradual up-regulation from the appearance of autoantibodies to the onset of T1DM.Conclusions These results indicate that CD274 up-regulation in T1DM is correlated with disease pathogenesis. PD-L1 might play a protective role in preventing the pancreatic islets from autoimmune destruction, which may help researchers find strategies for preventing the destruction process of pancreas beta-cells in T1DM.