Influenza virus infection-induced gene expression changes of regional B cells are mediated at least in part through type I Interferon:
Influenza virus infection causes global respiratory tract B cell response modulation via innate immune signals.
Sex, Specimen part
View SamplesExperiment 1: U133A arrays (2) hybridized to duplicate sscDNA samples prepared from 20 ng Clontech UHR RNA
Increased DNA microarray hybridization specificity using sscDNA targets.
No sample metadata fields
View SamplesOur study demonstrates that neutrophils infiltrate early-stage PTEN-deficient uterine tumors and oppose tumor growth and malignant progression by inducing detachment and ultimately promoting cell death of tumor cells. This RNA-seq study examined the expression profiles of these uterine epithelial tumor cells in the presence versus absence of neutrophil infiltration. Overall design: Tumor cells from 4-week-old tumor-bearing neutrophil-sufficient versus -deficient mice were isolated by fluorescence activated cell sorting, RNA was isolated, and expression profiles were analyzed by deep sequencing.
Neutrophils Oppose Uterine Epithelial Carcinogenesis via Debridement of Hypoxic Tumor Cells.
Age, Specimen part, Subject
View SamplesThis series represents isolated alveolar macrophages from human subjects.
A distinctive alveolar macrophage activation state induced by cigarette smoking.
No sample metadata fields
View SamplesPatients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.
Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
Sex, Age, Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The transcriptional regulator Aire coopts the repressive ATF7ip-MBD1 complex for the induction of immunotolerance.
Specimen part, Cell line
View SamplesHEK 293 cells were transiently transfected with plasmids expressing Vector only(PCMV), Aire, or MBD-VP16 with the goal of comparing the global gene expression profiles in the Aire and MBD-VP16 groups
The transcriptional regulator Aire coopts the repressive ATF7ip-MBD1 complex for the induction of immunotolerance.
Specimen part, Cell line
View SamplesWe compare the transcription profiles of IL-5-reporter marked ILC2s and Th2 cells sorted from mouse lung tissue after Nippostrongylus brasiliensis infection Overall design: mRNA sequencing comparing material from 2 cell populations sorted from the lungs of 7 Red5/Red5 mice, comprising 2 independent infections, 14 days after N.b. infection
A tissue checkpoint regulates type 2 immunity.
No sample metadata fields
View SamplesWe collected airway epithelial brushings for microarray analysis from 42 asthmatics and two control groups 28 healthy subjects and 16 smokers. A subgroup of 32 asthmatics completed a randomized placebo-controlled trial of fluticasone propionate in which collection of brushings was repeated after 1 week of treatment.
Genome-wide profiling identifies epithelial cell genes associated with asthma and with treatment response to corticosteroids.
Disease
View SamplesMicroRNAs (miRNAs) are important regulators of cell fate decisions in immune responses. They act by coordinate repression of multiple target genes, a property that we exploited to uncover regulatory networks that govern T helper-2 (Th2) cells. A functional screen of individual miRNAs in primary T cells uncovered multiple miRNAs that inhibited Th2 cell differentiation. Among these were miR-24 and miR-27, miRNAs coexpressed from two genomic clusters, which each functioned independently to limit interleukin-4 (IL-4) production. Mice lacking both clusters in T cells displayed increased Th2 cell responses and tissue pathology in a mouse model of asthma. Gene expression and pathway analyses placed miR-27 upstream of genes known to regulate Th2 cells. They also identified targets not previously associated with Th2 cell biology which regulated IL-4 production in unbiased functional testing. Thus, elucidating the biological function and target repertoire of miR-24 and miR-27 reveals regulators of Th2 cell biology. Overall design: Gene expression analysis of miRNA-deficient mouse CD4+ T cells transfected with miRNA mimics twice over a 5 day in vitro culture in the presence of low amounts of exogenous IL-4 (10U/ml). Cells transfected with either miR-23, miR-24 or miR-27 were compared to cells transfected with a control mimic. Data are from at least biologic triplicates.
MicroRNAs 24 and 27 Suppress Allergic Inflammation and Target a Network of Regulators of T Helper 2 Cell-Associated Cytokine Production.
Cell line, Subject
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