摘要
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.
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.
基金
This work was supported by grants from the National Natural Science Foundation of China （No. 81170725, 81070672, 81000316）, the European Foundation for the Study of Diabetes （No. EFSD/CDS/Lilly-2010）, the Key Project of Science and Technology Department of Hunan Province of China （No. 2010SK2007）, Hunan Provincial Natural Science Foundation of China （No. 11JJ7005）, the National Department Public Benefit （Health） Research Foundation of China （No. 201002002）, Research Fund for the Doctoral Program of Higher Education of China （No. 200805331018）. There are no financial/commercial conflicts of interests involving in this study.
