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 IL1RAP were verified and consistent with changes in microarray results. NK cell activity was decreased in F1D. 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-α signaling. CONCLUSIONS: These results identify several genes indicating possible mechanisms in F1D. NK cell dysfunction resulting from changes in expression of TLR9, ELF4 and IL1RAP, and pathways of interleukin-1 and tumor necrosis factor-α signaling might be involved in F1D through inducing β-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 IL1RAP were verified and consistent with changes in microarray results. NK cell activity was decreased in F1D. 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-α signaling. CONCLUSIONS: These results identify several genes indicating possible mechanisms in F1D. NK cell dysfunction resulting from changes in expression of TLR9, ELF4 and IL1RAP, and pathways of interleukin-1 and tumor necrosis factor-α signaling might be involved in F1D through inducing β-cell dysfunction.