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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Relation between T CD4+: Regulatory cells and IL-2 producing cells

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Antonio Freitas

PROVIDER: E-GEOD-54686 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Quorum sensing in CD4+ T cells homeostasis : IL-2 coordinates the interplay between IL-2p and regulatory T cells.

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

Relation between T CD4+: Regulatory cells and IL-2 producing cells

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

A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice

2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress

Analysis of cord blood CD4T cells

Project description:Purified CD4 T cells isolated from the cord blood were divided in subsets according to IL2R, IL7R and chemokine receptors (CCR6, CXCR3 and CCR4) and compared by whole genome microarray analysis. CD4 T cell memory subsets and Naive T cell collected from 3 donors (#480, #487, #488)

2014-06-04 | E-GEOD-51133 | biostudies-arrayexpress

Fluorochrome-based definition of naturally occurring Foxp3+ regulatory T cells of intra- and extrathymic origin

Project description:Here, we report on experiments in double-transgenic mice, in which RFP is expressed in all Foxp3+ Treg cells, whereas Foxp3-dependent GFP expression is exclusively confined to intrathymically induced Foxp3+ Treg cells. This novel molecular genetic tool enabled us to faithfully track and characterize naturally induced Treg cells of intrathymic (RFP+GFP+) and extrathymic (RFP+GFPM-bM-^HM-^R) origin in otherwise unmanipulated mice. These experiments directly demonstrate that extrathymically induced Treg cells substantially contribute to the overall pool of mature Foxp3+ Treg cells residing in peripheral lymphoid tissues of steady-state mice. Furthermore, we provide evidence that intra- and extrathymically induced Foxp3+ Treg cells represent distinct phenotypic and functional sublineages. CD4+CD25+ RFP+GFP- and CD4+CD25+ RFP+GFP+ T cells from pooled lymph nodes and pooled spleens of 20 mice were FACS sorted for RNA extraction and hybridization on Affymetrix microarrays in duplicates.

2014-07-09 | E-GEOD-59202 | biostudies-arrayexpress

RNA-seq of murine CD4 T cells after pentanoate treatment compared to untreated control

Project description:To analyse the influence of pentanoate on the differentiation of naive CD4 T cells under Th17 inducing conditions, murine CD4 T cells were isolated from spleen and lymphnodes of FIR/TIGER mice (IL-10 (GFP) - Foxp3 (RFP) - Reporter mice). The T cells were kept for 3 days under Th17 inducing conditions either with 4 mM pentanoate or without pentanoate (control).

2019-01-15 | E-MTAB-6114 | biostudies-arrayexpress

Murine HIV-gagP24 CD8 T cells: bone marrow vs Lymph node

Project description:Transcriptional profiling to examine differences resulting from priming of virus-specific CD8 T cells in draining lymph node and in bone marrow, following intradermal injection of modified virus Ankara (MVA)-HIV gag. Transcriptional profiling of mouse pentamer H2kD-AMQMLKETI (HIV-gagP24) CD8 T cells from draining lymph nodes(LN) and bone marrow (BM ) 5 days following intradermal injection of MVA-HIV gag, and compared to naive (CD62L Hi CD44 int) CD8+ T cells from lymph node of naive mice (NTc). Three-condition experiment, BM, LN and NTc. Experimental replicates: 5 BM, 5 LN, 5 NTc, RNA pooled from 3 independant experiments of 5 mice each.

2012-10-23 | E-GEOD-41736 | biostudies-arrayexpress

RNA-seq analysis of transcriptomes of WT and Foxp3∆2 Treg cells in spleen and LNs

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2023-07-01 | GSE208094 | GEO

Global Gene Expression of hematopoietic stem cells expressing endogenous NrasG12D/G12D, NrasG12D/+, Nras+/+

Project description:Oncogenic NRAS mutations are frequently identified in human myeloid leukemias. In mice, expression of endogenous oncogenic Nras (NrasG12D/+) in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN). However, acute expression of NrasG12D/+ in a pure C57BL/6 background does not induce hyperactivated GM-CSF signaling or increased proliferation in myeloid progenitors. It is thus unclear how NrasG12D/+ signaling promotes leukemogenesis. Here we show that hematopoietic stem cells (HSCs) expressing NrasG12D/+ serve as MPN initiating cells. They undergo moderate hyperproliferation with increased self-renewal. The aberrant NrasG12D/+ HSC function is associated with hyperactivation of ERK1/2 in HSCs. Conversely, downregulation of MEK/ERK by pharmacological and genetic approaches attenuates the cycling of NrasG12D/+ HSCs and prevents the expansion of NrasG12D/+ HSCs and myeloid progenitors. Our data delineate critical mechanisms of oncogenic Nras signaling in HSC function and leukemogenesis. three NrasG12D/G12D HSCs samples, three NrasG12D/+ HSCs samples, two Nras+/+ HSCs control samples.

2013-05-29 | E-GEOD-46948 | biostudies-arrayexpress

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