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Transcription profiling by sequencing of murine MyD88 -/- and MyD88 +/+ mTECs stimulated with a TLR9 ligand

ABSTRACT: Transcription profiling by sequencing of murine MyD88 -/- and MyD88 +/+ mTECs stimulated with a TLR9 ligand

PROVIDER: PRJEB32959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3365980.fastq.gz	Fastqsanger.gz
	ERR3365990.fastq.gz	Fastqsanger.gz
	ERR3365981.fastq.gz	Fastqsanger.gz
	ERR3365991.fastq.gz	Fastqsanger.gz
	ERR3365982.fastq.gz	Fastqsanger.gz

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Transcription profiling by sequencing of murine MyD88 -/- and MyD88 +/+ mTECs stimulated with a TLR9 ligand

Project description:We compared in vitro mTECs-high stimulated with TLR9 ligand CpG ODN (1826) or non stimulated from MyD88 -/- and MyD88 +/+ mice: Thymi were enzymaticaly digested, cells were MACS enriched for CD45- fraction, and FACS sorted using BD Influx sorter. mTECs-high were gated as EpCAM+CD11c-Ly51-MHCII+CD80+. Cell from MyD88 -/- and MyD88 +/+ mice were incubated in RPMI with or without CpG ODN (1826) for 24 hours. Total RNA was isolated using RNeasy Plus Micro Kit (Qiagen). 4 samples per condition were used.

2020-03-20 | E-MTAB-8025 | biostudies-arrayexpress

Oncogenic MyD88 Mutants Require Toll-like Receptors

Project description:In the activated B-cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), the most frequent gain-of-function mutations target MyD88, a signaling adapter for Tolllike receptors (TLRs). The most prevalent oncogenic mutant, MyD88 L265P, occurs in 29% of cases and is the most active in engaging the NF-kappaB pathway. Here we show that MyD88 mutants do not function autonomously, but rather require TLR7, TLR9, and to a lesser extent, TLR4 to promote the survival of ABC DLBCL cells. Unlike wild type MyD88, MyD88 mutants associate constitutively with TLR7 and TLR9 in ABC DLBCL cells. Like ligand-induced TLR7/9 signaling in normal immune cells, the survival of ABC DLBCL cell lines depends upon translocation of TLR7 and TLR9 to acidic endolysosomes, where proteolytic processing of their ligand binding ectodomains is required for their oncogenic signaling. ABC DLBCL viability also depends upon CD14, a co-receptor for TLR7 and TLR9 that promotes engagement of nucleic acid ligands by these receptors. Point mutations in the TLR7 or TLR9 ectodomains that abrogate ligand binding and/or signaling were incapable of sustaining ABC DLBCL survival. An inhibitory oligonucleotide that suppresses TLR9 responses in normal B cells blocked NF-kappaB signaling and survival of ABC DLBCL lines. Together, these data suggest that an endogenous TLR ligand may play a pathogenic role in ABC DLBCL and provide a rationale for targeting TLR signaling to improve therapy of this aggressive lymphoma. Gene expression was analyzed using Agilent human 2-color 4X44K oligo gene expression arrays. Cell line, TMD8 ABC-DLBCL, was infected with control (shControl, Cy3), shLTR7 (Cy5) or shLTR9 (Cy5) and changes in gene expression were monitored on day 1 and day 2 after induction of the shRNA with doxycycline, co-hybridizing control and experimental samples (Cy3+Cy5), for a total of 4 arrays.

2014-05-21 | E-GEOD-47147 | biostudies-arrayexpress

Oncogenic MyD88 Mutants Require Toll-like Receptors

2014-05-21 | GSE47147 | GEO

E-MTAB-8025

Project description:Transcription profiling by sequencing of murine MyD88 -/- and MyD88 +/+ mTECs stimulated with a TLR9 ligand

2019-09-09 | E-MTAB-8025 | ExpressionAtlas

Single Cell RNA sequencing of TLR9 ligand (CpG oligonucleotide) and TLR2/4 ligand (LPS)-treated mouse gingiva

Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of TLR9 ligand (CpG oligonucleotide) and TLR2/4 ligand (LPS)-treated mouse maxilla. Method: TLR9 ligand or TLR2/4 ligand was topically applied to the mouse palatal gingiva. Mouse palatal gingiva was harvested at 4 days after topical application. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.

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Transcription profiling of mouse LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- animals

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

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Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice.

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ATAC-seq analysis of aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of systemic lupus erythematosus.

Project description:Purpose: The goal of this study was to assess if TLR9 deficiency (TLR9-/-) or TLR9 incapacity to signal through MyD88 would differentially influence the epigenetic states of ABC, in a B cell intrinsic manner. Methods : Mixed bone marrow chimeras of one-third each TLR9+/+ CD45.1/2, TLR9-/- CD45.1/1 and TLR9P915H/P915H CD45.2/2 were generated on the MRL/lpr background. From each recipient, ABC were sorted with respect to the CD45 congenic markers at [20 weeks] post chimerism. DNA was isolated using a protocol adapted from Corces et al. Samples were sequenced to obtain 20M 2x75 bp paired-end reads using an Illumina NextSeq 550 sequencer (Illumina, Inc, California, USA). Results: The majority of differences in open chromatin regions were observed between TLR9-/- and TLR9P915H ABCs. This must reflect the MyD88-independent regulatory function of TLR9 (lost in TLR9-/- and present in TLR9P915H).

2022-08-03 | GSE202103 | GEO

RNA-seq analysis of follicular (FO), marginal zone (MZ) and aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of SLE

Project description:Purpose: The goal of this study was to assess if TLR9 deficiency (TLR9-/-) or TLR9 incapacity to signal through MyD88 would differentially influence the gene programs of B cell subsets, in a B cell intrinsic manner. Methods : Mixed bone marrow chimeras of one-third each TLR9+/+ CD45.1/2, TLR9-/- CD45.1/1 and TLR9P915H/P915H CD45.2/2 were generated on the MRL/lpr background. From each recipient, three B cell subsets, FO, MZ and ABC were sorted with respect to the CD45 congenic markers at [x weeks] post chimerism. RNA was isolated using the RNeasy Plus Micro Kit (QIAGEN). Samples were sequenced using NovaSeq 6000 flowcell (Illumina, Inc, California, USA) with 100 bp paired-end reads (20 million reads per sample) and aligned to the mm10 genome using the STAR aligner. Results: ABCs showed the most transcriptional differences among TLR9 genotypes. TLR9P915H and TLR9WT ABC transcriptomes were much more similar to each other than to those of TLR9-/- mice, sharing 246 of 381 DEGs, even though TLR9P915H B cells could not signal via MyD88. These included a number of genes encoding for inhibitory or anti-inflammatory pathways, suggesting that TLR9 could induce a regulatory signal independently of MyD88.

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Effect of CXCL4 on TLR9-induced B cells

Project description:CXCL4 is a cationic peptide that binds to TLR9-ligand oligonucleotide, resulting in an inhibition of TLR9 response in B cells

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