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| Dataset Title | Description | Link |
| DOCK8 is critical for the survival and function of NKT cells [NKT_CD103+] | Analysis of DOCK8 deficient animals revealed a novel marker of NKT cell development, the integrin CD103. The role of CD103 was further investigated by RNA microarray comparing CD103 negative versus positive NKT cells. | GSE44815 |
| DOCK8 is critical for the survival and function of NKT cells [DOCK8_CPM_NKT] | Analysis of DOCK8 deficient animals revealed a key role for this protein the survival and maintenance of natural killer T cells. This work lead to the identification of genes regulated by the guanine exchange factor, DOCK8. | GSE44814 |
| Human primary airway epithelial cell cultures infected with human- and swine-origin influenza viruses | Cultures of primary human airway epithelial cells (HAE cells) were exposed to an MDCK equivalent MOI of 0.01 of several swine- and human-origin influenza viruses and RNA was extracted at the 12, 16, and 24 hours post infection. | GSE41475 |
| Mutagenetix – A database of mutations and phenotypes induced by ENU | A database of mutations and phenotypes induced by ENU | mutagenetix.utsouthwestern.edu |
| Gene expression data from Mycobacterium tuberculosis-infected WT and miR-155-/- bone-marrow derived macrophages [timecourse] | How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages. | GSE79731 |
| Gene expression data from Mycobacterium tuberculosis-infected WT and miR-155-/- bone-marrow derived macrophages [validation] | How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages. | GSE79732 |
| Host response in cells from broncho-alveolar lavage (BAL) isolated from mice infected with influenza virus (PR8) and/or Staphylococcus aureus (Newman) | Array analysis of total RNA from broncho-alveolar lavage (BAL) from mice infected with influenza virus (PR8) and/or Staphylococcus aureus (Newman) | GSE83359 |
| Multiscale representation of genomic signals | ChIP-seq data of six proteins in primary murine bone marrow macrophage cells (BMMs) under unstimulated and lipopolysaccharide (LPS) stimulated conditions. Amongst these six proteins were three transcription factors (TFs), ATF340, NFκB/p50 and NFκB/p65, all of which are involved in regulating macrophage activation by microbial molecular components such as LPS. The other three ChIP-seq targets were RNA polymerase II (Pol II), and two chromatin modification marks: acetylation of histone H4 (H4ac) and tri-methylation of histone H3 lysine 27 (H3K27me3). | GSE54414 |
| Impairment of organ-specific T cell negative selection by diabetes susceptibility genes: analysis by mRNA profiling | Analysis of two thymic populations – early single positive thymocytes (CD4+CD8lowCD69+TCRhi) and early double positive thymocytes (CD4+CD8+CD69-TCRlow). Samples purified from the 3A9 TCR transgenic (TCR) to characterise positive selection and the 3A9 TCR x insHEL double transgenic (Dbl) to characterise negative selection towards an Aire-dependent organ-specific antigen. Both the non autoimmune C57BL10.H2k (B10) and autoimmune Non obese diabetic (NOD) strains were analysed in this method. Three biological replicates were used for each of these eight different groups. | GSE3997 |
| Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses | 12 microarrays of BMDM from wildtype C57BL/6 and Foxo3 knockout mice, unstimulated and stimulated with Poly(I:C) in triplicate. Three ChIP-Seq data sets in unstimulated BMDM; immunoprecipitation of Foxo3a in wildtype, and immunoprecipitation of acetylated histone H4 in both wildtype and Foxo3 knockout cells. | GSE37052 |
| The role of Ch25h in the macrophage response to poly(I:C) (bone-marrow-derived macrophages) | 24 RNA samples from murine bone-marrow-derived macrophages were analyzed using Agilent microarrays. Macrophages from C57BL/6 and Ch25h-/- mice were analyzed after mock stimulation or stimulation with 6ug/mL poly(I:C) or for 6 or 18 hours. For each condition, three biological replicates (macrophages derived from independent mice) were analyzed. | GSE54062 |
| The role of Ch25h in the macrophage response to poly(I:C) (Let1a) | 14 RNA samples from murine Let1a cells (immortalized airway epithelial cells) were analyzed using Agilent microarrays. Cells from C57BL/6 and Ch25h-/- mice were analyzed after mock stimulation or stimulation with 6ug/mL poly(I:C) or 5μM 25-Hydroxycholesterol for 6 or 18 hours. For each condition, two biological replicates were analyzed. | GSE54063 |
| HIV-1 infection of human monocyte-derived dendritic cells with and without the integrase inhibitor, Raltegravir | Myeloid dendritic cells (DCs) have the innate capacity to sense pathogens and orchestrate immune responses. However, DCs do not mount efficient immune responses some retroviruses such as HIV-1, due to potent restriction at the level of reverse transcription. Here, we uncover that when reverse transcription is allowed to proceed, DCs detect HIV-1 in distinct phases, before and after integration. Blocking integration suppressed, but did not abolish, activation of the transcription factor, IRF3, interferon responses, and DC maturation. The cytoplasmic DNA sensor, cGAS, and the E3 ligase, TRIM5, were both required for these responses. Consistent with two stages of innate activation, HIV-1 altered host chromatin accessibility before and after integration. DCs were derived from the peripheral blood from two deidentified human donors and infected with a single-cycle HIV-1 reporter virus (HIV-GFP) in the presence of Vpx, with and without Raltegravir. RNA expression was measured at 0, 8, 16, 20, 24, 28, 32, and 40 hours after infection. At 0, 16, 32, and 48 hours after infection, live cells were sorted and then prepped for an Assay for Transposase-Accessible Chromatin with high-throughput Sequencing (ATAC-Seq). | GSE100377 |