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FOXP3+ Regulatory T Cells Require TBET to Regulate Activated CD8+ T Cells During Recovery from Influenza Infection

ABSTRACT: FOXP3+ Regulatory T Cells Require TBET to Regulate Activated CD8+ T Cells During Recovery from Influenza Infection

PROVIDER: PRJNA1117002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29195107.fastq.gz	Fastqsanger.gz
	SRR29195111.fastq.gz	Fastqsanger.gz
	SRR29195112.fastq.gz	Fastqsanger.gz
	SRR29195114.fastq.gz	Fastqsanger.gz

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FOXP3+ Regulatory T Cells Require TBET to Regulate Activated CD8+ T Cells During Recovery from Influenza Infection

Project description:Our results demonstrate that TBET+ Treg cells regulate the numbers of activated CD8+ T cells expressing CD69 in the lung following influenza infection. Trm cells accumulated independently of Treg cells but mirrored transcriptional changes observed in activated CD8+ T cells following Treg cell depletion.

2025-06-10 | GSE268387 | GEO

Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. NaÃ¯ve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection

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PD-1 through asparaginyl endopeptidase regulates FoxP3 Stability in Induced Regulatory T cells

Project description:CD4+ T cell differentiation into multiple T helper lineages is critical for optimal adaptive immune responses. This report identified a novel intrinsic mechanism by which PD-1 signaling imparted regulatory phenotype to FoxP3+ Th1 cells (denoted as Tbet+iTregPDL1 cells) and iTregs. Tbet+iTregPDL1 cells were capable of preventing inflammation in murine models of experimental colitis and experimental graft versus host disease. PDL-1 binding to PD-1 imparted regulatory function to Tbet+iTregPDL1 cells and iTregs by specifically downregulating an endolysosomal protease asparaginyl endopeptidase (AEP) AEP regulated FoxP3 stability and blocking AEP imparted regulatory function in Tbet+iTregs cells. Also AEP-/- iTregs significantly inhibited GvHD and maintained FoxP3. Furthermore, PD-1 mediated FoxP3 maintenance in Tbet+Th1 cells occurred both in tumor infiltrating lymphocytes (TIL) and during chronic viral infection. Collectively, this report has identified a novel intrinsic function for PD-1 in converting Th1 cells into Tregs through an intrinsic proteolytic pathway

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Tbet-Eomes

Project description:Tbet-Eomes

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Tbet regulates the accessible chromatin of Be1 B cells

Project description:To investigate the role of Tbet in B cell differentiation to "effector-like" antibody secreting cells (ASC's) we utilized an ex vivo culture system to differentiate B cells in the presence of Th1 (Be1) or Th2 (Be2) polarized T cells. To determine the role of Tbet in Be1 cell differentiation we performed ATAC-seq on Wt Be1 and Tbet negative (TbetNeg) Be1 cells and Wt Be2 and Tbet negative (TbetNeg) Be2 cells. Collectively, these data show that T-bet serves as master regulator for the Be1 cell fate and is required to program chromatin accessibility during ASC differentiation in Be1 cells.

2019-04-29 | GSE118984 | GEO

Kinetics of Tbet+ B cells during LCMV infection

Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.

2022-01-27 | GSE150139 | GEO

Kinetics of Tbet+ B cells during LCMV infection

2022-01-27 | GSE192765 | GEO

Foxp3 ablation in peripheral mature regulatory T cells

Project description:Analysis of Foxp3 ablated peripheral regulatory T cells. Regulatory T cells require the expression of the transcription factor Foxp3 for thymic development. It is not known whether continuous expression of Foxp3 is required for the maintained function of mature regulatory T cells in the periphery. Results indicate changes to the regulatory T cell developmental program in the absence of Foxp3. Keywords: genetic modification

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Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was important even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. Naïve, Tbet+, and Tbet- Memory B cells were assayed for gene expression

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Tbet regulates the transcriptional programming of Be1 B cells.

Project description:To investigate the role of Tbet in B cell differentiation to "effector-like" antibody secreting cells (ASC's) we utilized an ex vivo culture system to differentiate B cells (Be1 cells) in the presence of Th1 polarized T cells. To determine the role of Tbet in Be1 cell differentiation we performed RNA-seq on Wt Be1 and Tbet negative (TbetNeg) Be1 cells. Collectively, these data show that T-bet serves as master regulator for the Be1 cell fate and is required for induction of genes required for ASC differentiation in Be1 cells.

2019-04-29 | GSE83697 | GEO

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