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Gene expression analysis of CD11c+ splenic DCs.

ABSTRACT: The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE61559 | GEO | 2014/09/19

SECONDARY ACCESSION(S): PRJNA261454

REPOSITORIES: GEO

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Gene expression analysis of CD11c+ splenic DCs.

Project description:The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype. CD11c+ cell sorted splenic DCs were isolated from 8 week old WT and Atg16L1 hypomorphic mice from spleens of untreated mice and were placed directly into TRIzol LS (Invitrogen). mRNA was isolated, amplified, and hybridized to an Affymetrix GeneChip (MOE430A).

2014-09-19 | E-GEOD-61559 | biostudies-arrayexpress

Gene expression analysis of CD11c+ splenic DCs day 7 after allo-HSCT.

2014-09-19 | GSE61560 | GEO

Gene expression analysis of CD11c+ splenic DCs day 7 after allo-HSCT.

Project description:The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype. CD11c+ cell sorted splenic DCs were isolated from 8 week old WT and Atg16L1 hypomorphic mice from spleens of allo-HSCT recipients on day 7 were placed directly into TRIzol LS (Invitrogen). mRNA was isolated, amplified, and hybridized to an Affymetrix GeneChip (MOE430A).

2014-09-19 | E-GEOD-61560 | biostudies-arrayexpress

Splenic CD8+ and CD8- DCs

Project description:Analysis of gene expressions in mouse splenic dendritic cells (DCs). DCs were purified into two subsets, CD8-positive and -negative ones. DCs were expanded in vivo by injecting Flt3L-producing tumors into the backs of C57BL/6 mice. To expand DCs in vivo, Flt3L-producing B16 melanoma cells were injected to the backs of mice. Then, 10-12 days later, splenic DCs were enriched by MACS and purified into CD3-B220-CD8a+CD11c+ and CD3-B220-CD8a-CD11c+ cells by FACS cell sorter.

2009-02-01 | E-GEOD-13250 | biostudies-arrayexpress

CD11c+ splenic DCs

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-09-19 | GSE61561 | GEO

CD11c+ splenic DCs

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-09-19 | E-GEOD-61561 | biostudies-arrayexpress

Gene expression profile in CD11c+ splenic dendritic cells and CD11c+CD103+ dendritic cells from mesenteric lymph nodes (MLN) of mice with DC-specific targeting of TGFBR2

Project description:Transcriptome analysis of dentritic cells from the spleen (CD11c+) or MLN (CD11c+CD103+) of mice with DC-specific deletion of TGFBR2 gene, or their control littermates. TRGFR2 gene was deleted in dendritic cells using Cre/lox approach. Mice with this deletion develop spontaneous multi-organ autoimmune inflammation and die by 15 weeks of age. Splenic CD11c+ Dc were isolated by magetic cell sorting. MLN CD11c+CD103+ DC were flow sorted. RNA was isolated using RNAqueous-Micro kit (Ambion) and analyzed using Affymetrix Mouse Exon 1.0 ST Array

2012-07-25 | E-GEOD-39651 | biostudies-arrayexpress

Gene expression profile in CD11c+ splenic dendritic cells and CD11c+CD103+ dendritic cells from mesenteric lymph nodes (MLN) of mice with DC-specific targeting of TGFBR2

2012-07-26 | GSE39651 | GEO

The role of CD11c in dendritic cells

Project description:We cultured bone marrow derived dendritic cells from WT and CD11c KO mice. Then, a group of bone marrow dendritic cells were stimulated with LPS overnight. We obtained bone marrow derived dendritic cells with or without LPS stimulation and analyzed proteomics profiles.

2024-01-26 | PXD048907 |

Gene expression analysis of crypt base epithelial cells from WT and Nod2-/- mice

Project description:Nod2 has been extensively characterized as a bacterial sensor that induces an antimicrobial and inflammatory gene expression program. Therefore, it is unclear why Nod2 mutations that disrupt bacterial recognition are paradoxically among the highest risk factors for Crohn’s disease, which involves an exaggerated immune response directed at intestinal bacteria. Previous studies from our lab have shown that mice deficient in Atg16L1, another Crohns disease susceptibility gene, develop abnormalities in Paneth cells, specialized epithelial cells in the small intestine involved in antimicrobial responses. The goal of our study is to determine whether Nod2 deficiency leads to differences in the transcriptional profile of Paneth cells, ultimately leading to small intestinal inflammation.

2014-07-01 | GSE58948 | GEO

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