HLA-B27-associated inflammatory diseases remains one of the strongest HLA-disease known to date. HLA-B27-associated acute anterior uveitis has wide-ranging medical significance due to its ocular, systemic, immunologic, and genetic features. To investigate the genes and signalling pathways located upstream of the inflammatory processes in HLA-B27-associated acute anterior uveitis will help to know the mechanism of this disease. HLA-B27-positive and -negative monocytes isolated from human peripheral blood were stimulated with Vibrio cholera lipopolysaccharide (LPS). Gene expression microarrays were used to identify the differentially expressed genes, and they were analysed by a series of bioinformatics-based techniques.
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Specimen part, Treatment
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Specimen part
View SamplesThe study of the differential expression profile in bone tissues between Tnni2del175k mutant mice and their wild-type littermates using mRNA array.
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Specimen part
View SamplesAim:
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Sex, Specimen part
View SamplesAn increasing number of studies have demonstrated that miRNAs may act as oncogenes or anti-oncogenes in various types of cancer, including colon carcinoma (CC). However the clinical and biological signicance of miR663a in the prognosis of CC and its underlying mechanisms remain unknown.
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Cell line
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Sex, Specimen part, Cell line
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miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.
Age, Specimen part, Disease, Disease stage
View SamplesWe used a genome-wide coding gene expression profiling to identify a gene signature for the molecular classification or prognostic prediction of primary GBMs.
miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.
Age, Specimen part, Disease, Disease stage
View SamplesToxoplasma gondii is an obligate intracellular parasite which can cause toxoplasmosis. Surface and secreted proteins of T. gondii play important roles in infection and immunity, and also are antigen targets in immunological diagnosis and vaccine development. However, it is difficult to investigate identities and antigenicities of surface and secreted proteins due to limitation of surface protein extraction methods. In this study, a total of 785 potential surface and secreted proteins of T. gondii RH tachyzoites were identified using a method combination of biotin labeling, avidin chromatography isolation, and high flux proteomics (LC-MS/MS). Among the highly-expressed 65 proteins, 43 proteins (66%) were originally annotated as surface or secreted proteins in the released T. gondii genomes, which proved the method combination to be a credible strategy. Furthermore, the transcriptomic responses and cytokine secretions induced by the isolated proteins, the live T. gondii RH tachyzoites infection, and the live pathogenic E. coli infection, in the human peripheral blood monocyte THP-1 cell lines, were comparatively analyzed to reveal antigenicities and immunobiological properties of T. gondii surface and secreted proteins. The transciptomic profiles induced by the isolated proteins were similar to those induced by the live bacterium infection, but were different from those induced by the live parasite infection. Contrary to the low cytokine secretion induced by the live parasite infection, the isolated proteins induced significant cytokine and chemokines secretion. Especially, the secretions of several chemokines induced by the isolated proteins were even higher than those induced by the live bacterium infection. These data suggested that T. gondii surface and secreted proteins were effective antigens, while the live parasite could evade the host innate immunity. This study comprehensively revealed the identities and antigenicities of T. gondii surface and secreted proteins, which laid foundation for further screening new T. gondii antigens, developing immunological diagnosis methods, and studying host immune response to T. gondii infection.
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Cell line, Treatment
View SamplesIdiopathic pulmonary fibrosis (IPF) is a progressive lethal interstitial lung disease of unkown etiology with limited effective therapies. The pathogenic mechanisms of IPF remain unkown. Emerging evidences indicate that abnormal behaviors of fibroblasts in IPF are associated with a variety of genetic alterations and aberrant reactivation of developmental signaling pathways.
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Specimen part, Disease
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