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Genome-wide analysis of lung antigen presenting cells gene expression from cigarette smoke exposed mice

ABSTRACT: Lung antigen presenting cells isolated from wild type but not Spp1-/- mice induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung antigen presenting cells from cigarette smoke exposed mice. These genes may play crucial roles in directing Th1 and Th17 cells differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE30906 | GEO | 2011/08/01

SECONDARY ACCESSION(S): PRJNA144225

REPOSITORIES: GEO

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Genome-wide analysis of lung antigen presenting cells gene expression from cigarette smoke exposed mice

Project description:Lung antigen presenting cells isolated from wild type but not Spp1-/- mice induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung antigen presenting cells from cigarette smoke exposed mice. These genes may play crucial roles in directing Th1 and Th17 cells differentiation. Lung antigen presenting cells were isolated from lungs of two groups of wild type and Spp1-/- mice that have been exposed to cigarette smoke for 4 months. Total mRNA was extracted from these samples.

2011-07-31 | E-GEOD-30906 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.

2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress

Expression data from antigen-presenting cells (APCs)

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Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

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Expression data from antigen-presenting cells (APCs)

Project description:P25 is the major T cell epitope for Ag85B and enables them to induce P25-specific CD4+ Th1 cells. We used microarrays to examine the gene expression of antigen-presenting cells (APCs) stimulated with P25 and P25-specific CD4+ T cells. Splenic APCs from WT mice were cultured with P25 or medium in the presence of P25 TCR CD4+ T cells. After overnight culture, these APCs were enriched and total RNA was prepared using RNeasy (QIAGEN) according to the manufacturer's instructions. Mixed total RNA from three independent experiments was used for microarray analysis.

2012-03-01 | E-GEOD-36018 | biostudies-arrayexpress

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Project description:Transcriptional profiles of four different myeloid antigen presenting cell (APC) subsets (BDCA-1+ circulating myeloid dendritic cells, CD14+ monocytes, and in vitro generated immature and mature monocyte-derived dendritic cells) were used for comprehensive transcriptome analysis. Based on the gene expression profiling data, a quantitative relationship between myeloid APC in functionally related gene spaces was established. Keywords = myeloid antigen presenting cells Keywords = dendritic cell subsets Keywords: repeat sample

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Phenotypes of Th lineages generated by the commonly used activation with anti-CD3/CD28 antibodies differ from those generated by the physiological activation with the specific antigen

Project description:T-helper (Th) lineages have been generated in vitro by activating CD4 cells with anti-CD3/CD28 antibodies during polarization. Physiologically, however, the generation of Th lineages is by activation with the specific antigen presented by antigen-presenting cells (APC). Here, we used TCR-transgenic mice to compare the phenotypes of Th1, Th9 and Th17 lineages when generated by either one of the two activation modes. Lineage Th cells specific against hen egg lysozyme (HEL), were adoptively transferred into recipient mice transgenically expressing HEL in their lens. Remarkable differences were found between lineages of Th1, Th9, or Th17, generated by either one of the two modes in their capacities to migrate to and proliferate in the recipient spleen and, importantly, to induce inflammation in the recipient mouse eyes. Substantial differences were also observed between the lineage pairs in their transcript expression profiles of certain chemokines and chemokine receptors. Surprisingly, however, close similarities were observed between the transcript expression profiles of lineages of the three phenotypes, activated by the same mode. Furthermore, Th cell lineages generated by the two activation modes differed considerably in their pattern of gene expression, as monitored by microarray analysis, but exhibited commonality with lineages of other phenotypes generated by the same activation mode. This study thus shows that (i) Th lineages generated by activation with anti-CD3/CD28 antibodies differ from lineages generated by antigen/APC and (ii) the mode of activation determines to a large extent the expression profile of major transcripts NaM-CM-/ve CD4+ T cells purified from spleen and lymph node cells of 3A9 mice were activated and polarized toward Th1, Th9, and Th17 lineages, under either plate bound anti-CD3/anti-CD28 (PBAB) or APC presented HEL protein (HA).

2014-02-13 | E-GEOD-54938 | biostudies-arrayexpress

Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis

Project description:Extracellular cold-inducible RNA-binding protein (eCIRP) is a key mediator of severity and mortality in sepsis. We found that stimulation of mouse bone marrow–derived neutrophils (BMDNs) with eCIRP generated a distinct neutrophil subpopulation, characterized by cell surface markers of both antigen-presenting cells and aged neutrophils as well as expression of IL-12, which we named antigen-presenting aged neutrophils (APANs). The frequency of APANs was significantly increased in the blood, spleen, and lungs of WT mice subjected to cecal ligation and puncture–induced sepsis but not in CIRP–/– mice. Patients with sepsis had a significant increase in circulating APAN counts compared with healthy individuals. Compared with non–APAN-transferred mice, APAN-transferred septic mice had increased serum levels of injury and inflammatory markers, exacerbated acute lung injury (ALI), and worsened survival. APANs and CD4+ T cells colocalized in the spleen, suggesting an immune interaction between these cells. APANs cocultured with CD4+ T cells significantly induced the release of IFN-γ via IL-12. BMDNs stimulated with eCIRP and IFN-γ underwent hyper-NETosis. Stimulating human peripheral blood neutrophils with eCIRP also induced APANs, and stimulating human neutrophils with eCIRP and IFN-γ caused hyper-NETosis. Thus, eCIRP released during sepsis induced APANs to aggravate ALI and worsen the survival of septic animals via CD4+ T cell activation, Th1 polarization, and IFN-γ–mediated hyper-NETosis.

2023-09-27 | GSE228482 | GEO

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