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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from cardiac CD11c+MHC II+ cells

ABSTRACT: We previously reported that a synthetic Nod1 ligand, FK565, induced coronary arteritis in mice similar to Kawasaki disease. However, the molecular mechanisms underlying this site-specific inflammation have remained elusive. In this study, we found that CD11c+MHC class II+ cells accumulated in the heart of FK565-treated mice prior to arteritis development. We used microarray analysis to detail gene expression of CD11c+MHC class II+ cells. To obtain gene expression profile of CD11c+MHC class II+ cells, we isolated these cells from hearts of FK565-treated mice. Briefly, female mice at 8weeks age were administered 500 μg of FK565 subcutaneously at day 0 and day 3. At day6, murine hearts were removed and digested with collagenase. CD11c+MHC II+ cells were sorted as PI–CD45+Ly6G–NK1.1–CD11b+CD11c+MHC II+ using FACS Aria cell sorter (BD Biosciences). Sorted cells were subjected to RNA preparation. Two independent replicates from ten mice were made.

ORGANISM(S): Mus musculus

SUBMITTER: Yoshitomo Motomura

PROVIDER: E-GEOD-60506 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from cardiac CD11c+MHC II+ cells

Project description:We previously reported that a synthetic Nod1 ligand, FK565, induced coronary arteritis in mice similar to Kawasaki disease. However, the molecular mechanisms underlying this site-specific inflammation have remained elusive. In this study, we found that CD11c+MHC class II+ cells accumulated in the heart of FK565-treated mice prior to arteritis development. We used microarray analysis to detail gene expression of CD11c+MHC class II+ cells.

2015-03-31 | GSE60506 | GEO

Expression data from Ly6G+ and Ly6G- dendritic cells (DC)

Project description:To investigate the functional properties of Ly6G+ DC, we employed GeneChip analysis to compare the gene expression profiles between Ly6G+ DC and Ly6C- DC. Crude bone marrow (BM) cells prepared from C57BL/6 mice were cultured in the presence of GM-CSF. On day 6, CD11c+/MHC II+/Ly6G+ cells and CD11c+/MHC II+/Ly6G- cells were simultaneously sorted from the same cultures by FACSAria. Total RNA were extracted and hybridized on Affymetrix microarrays.

2013-02-01 | E-GEOD-28408 | biostudies-arrayexpress

Expression data from self-deprived regulatory CD4 T cells

Project description:Disruption of TCR /MHC class II interactions leads rapidly to alterations of the common CD4 Treg transcriptional signature Self-deprived, non-functional Tregs were compare to fully functional Tregs by microarrays. Total T cells from the periphery of WT mice were adoptively transferred into CD3ε-/- recipient mice lacking or not MHC class II molecule expression (MHC II- or MHC II+ recipient mice, respectively). Five days later, peripheral Tregs transferred in MHC II - competent (CD4CD25B6) or - deficient (CD4CD25IIko) recipient were purified for RNA extraction and hybridization on Affymetrix microarrays.

2011-01-20 | E-GEOD-26714 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from cardiac CD11c+MHC II+ cells

| PRJNA258442 | ENA

RNA-Seq of steady-state and LPS stimulated splenic classical dendritic cells from wild type, germ-free and IFNAR knockout mice

Project description:The transcriptome of splenic classical dendritic cells (cDCs) (CD3- CD19- CD45+ MHC-II+ CD11c+) was compared in Wild Type (WT) mice, Germ Free (GF) mice and mice deficient for the Ifnar1 gene (IFNAR). Cells were isolated and sorted by flow cytometry to high purity. The cells were stimulated ex vivo with PBS or LPS. The results show remarkable similarities between the transcriptome of splenic cDCs in GF and IFNAR mice.

2018-06-30 | E-MTAB-5190 | biostudies-arrayexpress

Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses [Epigenetic CRISPRscreen]

Project description:There is increasing recognition of the prognostic significance of tumor cell major histocompatibility complex (MHC) class II expression in anti-cancer immunity. Relapse of acute myeloid leukemia (AML) following allogeneic stem cell transplantation (alloSCT) has recently been linked to MHC class II silencing in leukemic blasts; however, the regulation of MHC class II expression remains incompletely understood. Utilizing unbiased CRISPR-Cas9 screens, we identify that the C-terminal binding protein (CtBP) complex transcriptionally represses MHC class II pathway genes, while the E3 ubiquitin ligase complex component FBXO11 mediates degradation of CIITA, the principal transcription factor regulating MHC class II expression. Targeting these repressive mechanisms selectively induces MHC class II upregulation across a range of AML cell lines. Functionally, MHC class II+ leukemic blasts stimulate antigen-dependent CD4+ T cell activation and potent anti-tumor immune responses, providing fundamental insights into the graft-versus-leukemia effect. These findings establish the rationale for therapeutic strategies aimed at restoring tumor-specific MHC class II expression to salvage AML relapse post-alloSCT and also potentially to enhance immunotherapy outcomes in non-myeloid malignancies.

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Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses [RNA-Seq]

2022-10-02 | GSE189772 | GEO

Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses [CUT&TAG]

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Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses [Whole-genome CRISPRscreen]

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Rapid CLIP Dissociation from MHC II Promotes an Unusual Antigen Presentation Pathway in Autoimmunity

Project description:A number of autoimmunity-associated MHC class II proteins interact only weakly with the invariant chain-derived class II-associated invariant chain peptide (CLIP). CLIP dissociates rapidly from I-Ag7 even in the absence of DM, and this property is related to the type 1 diabetes-associated b57 polymorphism. We generated knock-in Non-obese Diabetic (NOD) mice with a single amino acid change in the CLIP segment of invariant chain in order to moderately slow CLIP dissociation from I-Ag7. These knock-in mice had a significantly reduced incidence of spontaneous type 1 diabetes and diminished islet infiltration by CD4 T cells, in particular T cells specific for fusion peptides generated by covalent linkage of proteolytic fragments within b cell secretory granules. Rapid CLIP dissociation enhanced presentation of such extracellular peptides, thus bypassing the conventional MHC class II antigen processing pathway. Autoimmunity-associated MHC class II polymorphisms therefore not only modify binding of self-peptides, but also alter the biochemistry of peptide acquisition.

2018-08-09 | GSE118322 | GEO

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