Gene expression changes in patients with fulminant type 1 diabetes

Background Fulminant type 1 diabetes （F1D） is a complex disease. Microarray analysis was used to identify gene expression changes and obtain understanding of the underlying mechanisms. Methods Microarray analysis was performed on peripheral blood mononuclear cells from six F1D patients and six match...

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Bibliographic Details
Published in:Chinese medical journal 2011-11, Vol.124 (22), p.3613-3617
Main Authors: Wang, Zhen, Zheng, Chao, Tan, Yu-Yu, Li, Yi-Jun, Yang, Lin, Huang, Gan, Lin, Jian, Zhou, Zhi-Guang
Format: Article
Language:English
Subjects:
Adult
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - metabolism
Female
Gene Expression Profiling
Humans
Male
Middle Aged
NK细胞活性
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Young Adult
基因表达
外周血单核细胞
患者
暴发性
白细胞介素-1
糖尿病
肿瘤坏死因子
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Summary:Background Fulminant type 1 diabetes （F1D） is a complex disease. Microarray analysis was used to identify gene expression changes and obtain understanding of the underlying mechanisms. Methods Microarray analysis was performed on peripheral blood mononuclear cells from six F1D patients and six matched healthy subjects. Real-time polymerase chain reaction was used to verify the differentially expressed genes. NK cell activity was detected by methyl thiazoleterazolium assay. Results Microarray analysis identified 759 genes differing in expression between F1D patients and controls at a false discovery rate of 0.05. Expression of TLR9, ELF4 and ILIRAP were verified and consistent with changes in microarray results. NK cell activity was decreased in FID. With use of a knowledge base, differentially expressed genes could be placed within different pathways with predicted functions including interleukin-1, and tumor necrosis factor-a signaling. Conclusions These results identify several genes indicating possible mechanisms in FID. NK cell dysfunction resulting from changes in expression of TLR9, ELF4 and IL1RAP, and pathways of interleukin-1 and tumor necrosis factor-a sianalino miaht be involved in F1D throuoh inducino B-cell dysfunction.
ISSN:0366-6999
2542-5641
DOI:10.3760/cma.j.issn.0366-6999.2011.22.003