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RNA-seq analysis of follicular (FO) and marginal zone (MZ) B cells, isolated from TLR9WT or TLR9-/- BALB/c mice, stimulated with TLR7 agonists (CL097, Invivogen) or left unstimulated .

ABSTRACT: RNA-seq analysis of follicular (FO) and marginal zone (MZ) B cells, isolated from TLR9WT or TLR9-/- BALB/c mice, stimulated with TLR7 agonists (CL097, Invivogen) or left unstimulated .

PROVIDER: PRJNA834734 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19052600.fastq.gz	Fastqsanger.gz
	SRR19052600_1.fastq.gz	Fastqsanger.gz
	SRR19052600_2.fastq.gz	Fastqsanger.gz
	SRR19052577.fastq.gz	Fastqsanger.gz
	SRR19052577_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of follicular (FO) and marginal zone (MZ) B cells, isolated from TLR9WT or TLR9-/- BALB/c mice, stimulated with TLR7 agonists (CL097, Invivogen) or left unstimulated .

Project description:Purpose: The goal of this study was to assess if increased TLR7 signaling could be seen in TLR9-/- compared to TLR9WT FO and MZ B cells. Methods : FO and MZ B cells from TLR9WT or TLR9-/- BALB/c mice were sorted using FACSaria. A minimum of 100,000 cells per B cell subsets were sorted. Sorted B cell subsets were stimulated for 4 hours at 0.25M/ml with TLR7 agonist CL097 (Invivogen) at 5µg/ml or left unstimulated. RNA was isolated using the RNeasy Plus Micro Kit (QIAGEN). Samples were sequenced on an Illumina Next-seq 2000 using a P3 200 cycle flowcell (Illumina, Inc) with 2 x 101 bp paired-end reads (20 million reads per sample). Results: There were no significant DEG (FDR > 0.05) following TLR7 stimulation between TLR9WT and TLR9-/- FO or MZ B cells.

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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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miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

Project description:We have analyzed miRNA expression profile in FO and MZ B cells to identified differentially expressed miRNAs between this two subsets that could be potencially involved in the regulation of terminal B cell differentiation Spleens from CD19-Creki/+Dicerfl/+ and CD19-Creki/+Dicerfl/fl mice were collected and after erythrocyte lysis, splenocytes were stained with anti-B220, anti-CD21 and anti-CD23 antibodies. B220+CD21brightCD23+ (MZ) and B220+CD21+CD23bright (FO) B cell populations were sorted and total RNA of purified populations was extracted with TRIzol. miRNA microarray hybridations were performed on Mouse miRNA Microarray platform (Agilent Technologies).

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Project description:Endosomal Toll-like receptors (TLRs) play an important role in the etiology of systemic autoimmune diseases such as SLE, where DNA- and RNA-associated autoantigens activate autoreactive B cells through TLR9- and TLR7-dependent pathways, respectively. Nevertheless, TLR9-deficient autoimmune prone mice develop more severe clinical disease, while TLR7-deficient and TLR7/9-double deficient autoimmune-prone mice develop less severe disease. To determine whether the regulatory activity of TLR9 is B cell intrinsic, we have now directly compared the functional properties of autoantigen activated WT, TLR9-deficient and TLR7-deficient B cells, in an experimental system where proliferation depends on BCR/TLR co-engagement. In vitro, TLR9-deficient cells are less dependent on survival factors for a sustained proliferative response than either WT or TLR7-deficient cells. The TLR9-deficient cells also preferentially differentiate toward the plasma cell lineage, as indicated by expression of CD138, sustained expression of IRF4, and other molecular markers of plasma cells. In vivo, autoantigen-activated TLR9-deficient cells give rise to greater numbers of autoantibody producing cells. Our results identify distinct roles for TLR7 and TLR9 in the differentiation of autoreactive B cells that explain the capacity of TLR9 to limit, and TLR7 to promote, the clinical features of SLE. AM14 WT, Tlr7-/-, Tlr9-/- and Tlr7/9-/- B cells were stimulated with PL2-3 for 0, 6, 24, and 42 hours, for a total of 16 samples.

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