Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA216373 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Many species of bacteria use quorum sensing to sense the amounts of secreted metabolites and adapt their growth according to their population density. We asked whether similar mechanisms would operate in lymphocyte homeostasis. We investigated the regulation of the size of Interleukin-2-producing CD4+ T-cell (IL-2p) pool using different IL-2-reporter mice. We found that in the absence of either IL-2 or regulatory CD4+ T-cells (Treg) the number of IL-2p-cells increases. Administration of IL-2 decreases the number of cells of the IL-2p-cell subset and pertinently, abrogates their ability to produce IL-2 upon in vivo cognate stimulation, while increasing Treg-cell numbers. We propose that control of the IL-2p-cell numbers occurs via a quorum-sensing-like feedback loop where the produced IL-2 is sensed by both the activated CD4+ T-cell pool and by Treg-cells, which reciprocally regulate cells of the IL-2p-cell subset. In conclusion, IL-2 acts as a self-regulatory circuit integrating the homeostasis of activated and regulatory T cells as CD4+ T-cells restrain their growth by monitoring IL-2 levels thereby preventing uncontrolled responses and autoimmunity. 2 populations of conventional CD4+ T cell are analysed. 5 replicates for each. GFP- is the control one.
2013-11-01 | E-GEOD-50149 | biostudies-arrayexpress
Project description:Many species of bacteria use quorum sensing to sense the amounts of secreted metabolites and adapt their growth according to their population density. We asked whether similar mechanisms would operate in lymphocyte homeostasis. We investigated the regulation of the size of Interleukin-2-producing CD4+ T-cell (IL-2p) pool using different IL-2-reporter mice. We found that in the absence of either IL-2 or regulatory CD4+ T-cells (Treg) the number of IL-2p-cells increases. Administration of IL-2 decreases the number of cells of the IL-2p-cell subset and pertinently, abrogates their ability to produce IL-2 upon in vivo cognate stimulation, while increasing Treg-cell numbers. We propose that control of the IL-2p-cell numbers occurs via a quorum-sensing-like feedback loop where the produced IL-2 is sensed by both the activated CD4+ T-cell pool and by Treg-cells, which reciprocally regulate cells of the IL-2p-cell subset. In conclusion, IL-2 acts as a self-regulatory circuit integrating the homeostasis of activated and regulatory T cells as CD4+ T-cells restrain their growth by monitoring IL-2 levels thereby preventing uncontrolled responses and autoimmunity.
2013-11-01 | GSE50149 | GEO
Project description:We previously proposed that lymphocyte homeostasis is achieved by a quorum-sensing like mechanism, based on the paracrine sensing of IL-2 by Foxp3(+) regulatory T CD4(+) cells. In turn, these cells will suppress IL-2 producing cells, thereby controlling the total number of T CD4(+) cells. As CD4(+) T regulatory cells are unable to produce IL-2, such control mechanism assumes the complete segregation of both lymphocyte subsets, that is to say they constitute distinct compartments. In the present study, we re-evaluate the above-described quorum-sensing mechanism by considering the non-exclusive possibility that a fraction of IL-2-producing cells might acquire regulatory function, implying the existence of a role for an autocrine sensing of IL-2 in the homeostasis of the regulatory compartment. According to the mouse models used in these experiments, RFP is used as a reporter for the Foxp3 expression. The transcription factor Foxp3 is the main hallmark of T CD4(+) regulatory cells. Therefore RFP(+) cells are associated to T CD4(+) regulatory cells. According to the mouse model, and our last publication (PMID: 24249704), the GFP is a reporter for cells that having activated the IL-2 locus within the last 2-3 weeks. This subset of cells is called IL-2p cells. 4 populations of conventional CD4+ T cell are analysed. 5 replicats for each.
2015-02-01 | E-GEOD-54686 | biostudies-arrayexpress
Project description:We previously proposed that lymphocyte homeostasis is achieved by a quorum-sensing like mechanism, based on the paracrine sensing of IL-2 by Foxp3(+) regulatory T CD4(+) cells. In turn, these cells will suppress IL-2 producing cells, thereby controlling the total number of T CD4(+) cells. As CD4(+) T regulatory cells are unable to produce IL-2, such control mechanism assumes the complete segregation of both lymphocyte subsets, that is to say they constitute distinct compartments. In the present study, we re-evaluate the above-described quorum-sensing mechanism by considering the non-exclusive possibility that a fraction of IL-2-producing cells might acquire regulatory function, implying the existence of a role for an autocrine sensing of IL-2 in the homeostasis of the regulatory compartment. According to the mouse models used in these experiments, RFP is used as a reporter for the Foxp3 expression. The transcription factor Foxp3 is the main hallmark of T CD4(+) regulatory cells. Therefore RFP(+) cells are associated to T CD4(+) regulatory cells. According to the mouse model, and our last publication (PMID: 24249704), the GFP is a reporter for cells that having activated the IL-2 locus within the last 2-3 weeks. This subset of cells is called IL-2p cells.
2015-02-01 | GSE54686 | GEO
Project description:IL-17A and F are critical cytokines in anti-microbial immunity but also contribute to auto-immune pathologies. Recent evidence suggests that they may be differentially produced by T-helper (Th) cells but the underlying mechanisms remain unknown. To address this question, a logical model containing 82 components and 136 regulatory links was developed and calibrated with original flow cytometry data using naive CD4+ T cells in conditions inducing either IL-17A or F. Model analyses led to the identification of the transcription factors NFAT2A, STAT5A and Smad2 as key components explaining the differential expression of IL-17A and IL-17F, with STAT5A controlling IL-17F expression, and an interplay of NFAT2A, STAT5A and Smad2 controlling IL-17A expression.
2021-04-06 | MODEL2101150001 | BioModels
Project description:Quorum signal uptake is an indispensable part of quorum sensing regulations. The coperative regulation of uptake repressor and kinase precisely signale the cells for quorum sensing uptake and terminate the quorum sensing signal production. We use the DNA microarray to detail the E. coli quorum sensing uptake reuglations and related gene regulations. Keywords: specific growth
2007-11-02 | GSE9203 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121386 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121287 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121284 | GEO