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Published in: Acta Diabetologica 8/2017

01-08-2017 | Original Article

Genome-wide gene expression profiling reveals that CD274 is up-regulated new-onset type 1 diabetes mellitus

Authors: Chen Fang, Yun Huang, Yufang Pei, Hong-hong Zhang, Xiaohong Chen, Heming Guo, Sicheng Li, Xiaoyan Ji, Ji Hu

Published in: Acta Diabetologica | Issue 8/2017

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Abstract

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 β-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 β-cells in T1DM.
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Metadata
Title
Genome-wide gene expression profiling reveals that CD274 is up-regulated new-onset type 1 diabetes mellitus
Authors
Chen Fang
Yun Huang
Yufang Pei
Hong-hong Zhang
Xiaohong Chen
Heming Guo
Sicheng Li
Xiaoyan Ji
Ji Hu
Publication date
01-08-2017
Publisher
Springer Milan
Published in
Acta Diabetologica / Issue 8/2017
Print ISSN: 0940-5429
Electronic ISSN: 1432-5233
DOI
https://doi.org/10.1007/s00592-017-1005-y

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