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Mitf regulates gene expression networks implicated in B cell homeostasis, germinal center responses, and tolerance

ABSTRACT: Mitf regulates gene expression networks implicated in B cell homeostasis, germinal center responses, and tolerance

PROVIDER: PRJNA1063205 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27480500_1.fastq.gz	Fastqsanger.gz
	SRR27480500_2.fastq.gz	Fastqsanger.gz
	SRR27480484_1.fastq.gz	Fastqsanger.gz
	SRR27480484_2.fastq.gz	Fastqsanger.gz
	SRR27480485_1.fastq.gz	Fastqsanger.gz

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Mitf regulates gene expression networks implicated in B cell homeostasis, germinal center responses, and tolerance

Project description:The microphthalmia transcription factor Mitf has been shown to regulate B cell activation and tolerance. However, the underlying B cell-specific mechanisms responsible, and those that distinguish Mitf from closely related Mitf/TFE (MiT) transcription factors Tfe3, Tfeb, and Tfec, remain obscure. Two complementary mouse models of Mitf and MiT deficiency – the Mitfmi-vga9/mi-vga9 systemic loss-of-function mutation, and B-cell specific MiT family inactivation via transgenic expression of a trans-dominant negative (TDN) protein (TDN-B) – were used to identify MiT family candidate target genes and pathways. Both models displayed spontaneous splenomegaly coincident with elevated plasma cell numbers, autoantibody titers, and proteinuria. These abnormalities appeared dependent on T helper cells, but independent of other non-B cell intrinsic effects of systemic Mitf inactivation. MiT inactivation in B cells augmented aspects of lupus-like autoimmune disease on the C57BL/6-Faslpr/lpr background. In both models, RNAseq of ex vivo resting B cells showed transcriptional upregulation of genes that control cell cycle, germinal center responses, and plasma cell differentiation. Among the genes strongly upregulated in both models were Socs6, Isp53 (Baiap1), S1pR2, and IgG2b/c. Mitf null B cells, but not TDN-B cells, showed evidence of type I interferon dysregulation implicating non-autonomous B-lymphocyte mechanisms caused by systemic absence of Mitf. These studies clarify Mitf's role as 1) a key regulator of a B cell intrinsic germinal center program that influences self-tolerance through novel target genes, and 2) a regulator of systemic inflammatory processes that can impact the B cell microenvironment.

2024-01-10 | GSE252903 | GEO

Proteome profiling of mouse germinal center B cells

Project description:Productive B cell responses are critical to protect a host from infection. The spleen and lymph nodes are populated by resting follicular B cells, which can enter germinal centers upon antigen encounter. Once in the germinal center, B cells migrate between the dark and light zones, where they undergo somatic hypermutation and selection, respectively. While germinal center B cells have been studied, an intense molecular understanding of these cells/subsets (and the differences between them) is lacking.

2020-04-06 | PXD015524 | Pride

ChIPseq analyses in germinal center B cells

Project description:Germinal center B cells were isolated from human tonsil tissue and crosslinked. ChIP was performed on two distinct pools of germinal center cells, each obtained from 3-5 donors. The experiment includes two biological replicates (germinal center cell pools from different donors). ChIP was performed on both pools and subject to library preparation and sequencing. Input DNA was sequenced for both pools.

2015-12-04 | E-GEOD-68349 | biostudies-arrayexpress

Deletion of miR-15a/16-1 in murine germinal center B-cells.

Project description:Given the tumor suppressing function of miR-15a/16-1 cluster, we studied its role in the germinal center B-cells that give rise to most lymphoid malignancies.

2021-09-09 | PXD021323 | Pride

ChIPseq analyses in germinal center B cells

2015-12-04 | GSE68349 | GEO

DNA Methylation Dynamics of Germinal Center B Cells Are Mediated by AID

Project description:Changes in DNA methylation are required for the formation of germinal centers (GC), but the mechanisms of such changes are poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated recently in DNA demethylation through its deaminase activity coupled with DNA repair. We investigated the epigenetic function of AID in vivo in germinal center B cells (GCB) isolated from wild type (WT) and AID-deficient (Aicda-/-) mice. We determined that the transit of B cells through the GC is associated with marked locus-specific loss of methylation and increased methylation diversity, both of which are lost in Aicda-/- animals. Differentially methylated cytosines (DMCs) between GCB and naïve B cells (NB) are enriched in genes that are targeted for somatic hypermutation (SHM) by AID and these genes form networks required for B cell development and proliferation. Finally, we observed significant conservation of AID-dependent epigenetic reprogramming between mouse and human B cells. ERRBS and RNA-seq of wild type and Aicda knockout murine naive and germinal center B cells. ERRBS of human naive and germinal center B cells

2015-09-15 | E-GEOD-71702 | biostudies-arrayexpress

The influence of TFEB on gene expression in primary murine germinal center and non-germinal center B cells

Project description:To investigate TFEB-dependent mRNA expression in murine B cells, FACS-sorted germinal center and non-germinal center B lymphocytes of B-cell-specific conditional TFEB KO mice and control littermates were subjected to RNA sequencing analysis

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Gene Expression Profiles of Germinal Center B Cells

Project description:We report the gene expression profiles of germinal center B cells obtained by FACS analyses of normal human lymph nodes. We used FACS analyses to isolate germinal center B cells from 3 different individuals with one individual sampled twice. The overall goal was simply to identify genes that are highly expressed or silent in these purified cell populations.

2009-07-31 | E-GEOD-16712 | biostudies-arrayexpress

RNA-seq analysis of gene expression profile in Setd2 WT and KO germinal center B cells and Phf19 WT and KO germinal center B cells

Project description:The goals of this study are to compare gene expression profiles of Setd2 WT and KO germinal center B cells and reveal the underlying mechanisms by which Setd2 regulates germinal center B cell responses. Further our study aims to compare gene expression profiles of Phf19 WT and KO germinal center B cells reveal the underlying mechanisms by which Phf19 regulates germinal center B cells responses. Finally, we combine the two profiles and investigate the relation shape betweeen Setd2 dependent regulation and Phf19 dependent regulation.

2024-09-14 | GSE184075 | GEO

Dynamic Regulation of Tfh Clonal Selection During the Germinal Center Reaction

Project description:The Germinal center is a dynamic microenvironment wherein B cells expressing high affinity antibody variants produced by hypermutation are selected for clonal expansion by limiting numbers of T follicular helper cells. Although a great deal is known about the mechanisms that control B cell selection in the germinal center, far less is understood about the clonal behavior of the T follicular helper cells that regulate this process. Here we report on the dynamic behavior of clones of T follicular helper cells during the germinal center reaction. We find that like germinal center B cells, T follicular helper cells undergo antigen dependent selection during the germinal center reaction resulting in differential proliferative expansion and contraction. Increasing the amount of antigen presented in the germinal center leads to increased T follicular cell division. Competition between T follicular helper cell clones is mediated by T cell receptor affinity for peptide-MHC ligand. Higher affinity T cells expanding preferentially in the germinal center show increased expression of genes downstream of the T cell receptor, genes required for metabolic reprogramming, cell division and cytokine production. These dynamic changes lead to dramatic remodeling of the functional T follicular cell repertoire during the germinal center reaction.

2020-03-19 | GSE147182 | GEO

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