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Beadarray expression analysis to identify how LILRB2 blockade may affect transcriptional networks in M(LPS) and M(IL4)

ABSTRACT: Beadarray expression analysis to identify how LILRB2 blockade may affect transcriptional networks in M(LPS) and M(IL4)

PROVIDER: PRJNA481786 | ENA |

REPOSITORIES: ENA

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Beadarray expression analysis to identify how LILRB2 blockade may affect transcriptional networks in M(LPS) and M(IL4)

Project description:We performed Illumina microarrays to identify how LILRB2 blockade may affect transcriptional networks in M(LPS) and M(IL4). To compare M(LPS) and M(IL4) populations helped define markers and pathway networks associated with M1 vs. M2-like functional phenotypes

2019-02-22 | GSE117340 | GEO

Wild type and ATG5-KO mouse dendritic cells exposed to interleukin-4 (IL4) and/or lipopolisaccharyde (LPS)

Project description:Male C57BL/6 normal and ATG5-KO mouse dendritic cells exposed to interleukin-4 (IL4) and/or lipopolisaccharyde (LPS) 24 samples representing the different biological combinations between wild type and ko cells exposed to IL4 and LPS (three replicates for each)

2015-06-16 | E-GEOD-56929 | biostudies-arrayexpress

Wild type and ATG5-KO mouse dendritic cells exposed to interleukin-4 (IL4) and/or lipopolisaccharyde (LPS)

Project description:Male C57BL/6 normal and ATG5-KO mouse dendritic cells exposed to interleukin-4 (IL4) and/or lipopolisaccharyde (LPS)

2015-06-16 | GSE56929 | GEO

Transcription profiling of mouse wild type or mir-155 deficient B cells after stimulation with LPS and IL4

Project description:Wild type or miR-155 deficient b cells from 5 individuals each were stimulated with LPS and IL4 for 24hs and profiled.

2007-11-21 | E-MEXP-1325 | biostudies-arrayexpress

Expression data from M(LPS+IFNγ) and M(IL4)

Project description:Human monocyte THP-1 cells obtained from ATCC were cultured in RPMI 1640 (Invitrogen, Carlsbad, CA) containing 10% FBS and supplemented with 10 mM Hepes (Gibco BRL). THP-1 was differentiated into macrophages by 24-h incubation with 160 nM phorbol 12-myristate 13-acetate (PMA; Sigma, St. Louis, MO) followed by 24-h incubation in RPMI medium. Macrophages were further polarized to M1 macrophages by incubation with 10 pg/ml of lipopolysaccharide (LPS; Sigma) and 20 ng/ml of interferon (IFN)-γ (R&D Systems, MN) and are referred to as M(LPS+IFN-γ) cells. M2 macrophages were obtained by incubation with 20 ng/ml of interleukin (IL)-4 (R&D Systems) and are referred to as M(IL4) cells. To test the represented polarization marker of PMA differentiated-THP-1 macrophages stimulated with 20 ng ml(-1) IFNγ + 10 pg ml(-1) LPS and 20 ng ml(-1) IL-4, which are known to influence macrophage polarization in vetro into the M1 and M2 state, respectively. We used microarrays to detail the gene expression pools to identify distinct M1 and M2 state during this process.

2017-02-28 | GSE95405 | GEO

RNA-seq gene expression profiling in resting murine B cells from WT or KMT2D knockout mice, before and after stimulation with LPS, IL4, and anti-CD180

Project description:Resting B cells were isolated from WT or KMTD KO mice by immunomagentic depletion of with anti-CD43 beads. Gene expression use determined by RNAseq in resting B cells or B cells stimulated with LPS, IL4, and anti-mouse CD180 for 3 days.

2017-08-28 | GSE68818 | GEO

IL4 promotes phagocytosis of murine leukemia cells counteracted by CD47 upregulation

Project description:Cytokines are key regulators of tumor immune surveillance by controlling immune cell activity. Here, we investigated whether interleukin 4 (IL4) has antileukemic activity via immune-mediated mechanisms in an in vivo murine model of acute myeloid leukemia driven by the MLL-AF9 fusion gene. Although IL4 strongly inhibited leukemia development in immunocompetent mice, the effect was diminished in immune-deficient recipient mice, demonstrating that the antileukemic effect of IL4 in vivo is dependent on the host immune system. Using flow cytometric analysis and immunohistochemistry, we revealed that the antileukemic effect of IL4 coincided with an expansion of F4/80+ macrophages in the bone marrow and spleen. To elucidate whether this macrophage expansion was responsible of the antileukemic effect, we depleted macrophages in vivo with clodronate liposomes. Macrophage depletion eliminated the antileukemic effect of IL4, showing that macrophages mediated the IL4-induced killing of leukemia cells. In addition, IL4 enhanced murine macrophage-mediated phagocytosis of leukemia cells in vitro. Global transcriptomic analysis of macrophages revealed an enrichment of signatures associated with alternatively activated macrophages and increased phagocytosis upon IL4 stimulation. Notably, IL4 concurrently induced Stat6-dependent upregulation of CD47 on leukemia cells, which suppressed macrophage activity. Consistent with this finding, combining CD47 blockade with IL4 stimulation enhanced macrophage-mediated phagocytosis of leukemia cells. Thus, IL4 has two counteracting roles in regulating phagocytosis in mice; enhancing macrophage-mediated killing of leukemia cells, but also inducing CD47 expression that protects target cells from excessive phagocytosis. Taken together, our data suggests that combined strategies that activate macrophages and block CD47 have therapeutic potential in AML.

2021-07-14 | GSE155048 | GEO

Alcanivorax sp. IL4

Project description:Alcanivorax sp. IL4 Genome sequencing

| PRJNA161065 | ENA

Expression in wild type and TgDREAM mouse B cells unstimulated or 2 days after LPS+IL4 stimulation

Project description:DREAM/KChIP-3 is a calcium-dependent transcriptional repressor highly expressed in immune cells. Transgenic mice expressing a dominant active DREAM mutant show reduced serum immunoglobulin levels. In vitro assays show that reduced immunoglobulin secretion is an intrinsic defect of transgenic B cells that occurs without impairment in plasma cell differentiation but with an accelerated entry in cell division and an increase in class switch recombination. B cells from DREAM knockout mice did not show any phenotype, due to compensation by endogenous KChIP-2. Expression arrays revealed modified expression of Edem1 and Derlin3, two proteins related to the ER-associated degradation pathway and of Klf9, a cell-cycle regulator. Our results disclose a function of DREAM and KChIP-2 in Ig subclass production in B lymphocytes. We used Affymetrix microarrays (GeneChip Mouse Genome 430 2.0) to compare global gene expression in wild type (WT) versus transgenic B cells (Tg), unstimulated and 2 days after LPS + IL4 stimulation. For ech type of sample three hybridizations were carried-out (independent biological replicates).

2010-12-07 | E-GEOD-16874 | biostudies-arrayexpress

Generation of macrophages that are profoundly pro-remyelinating through unexpected activation cues

Project description:Excessive inflammation within the central nervous system is injurious, but an immune response is also required for its repair. Macrophages are versatile cells that adopt different properties depending upon their microenvironment. Exposing macrophages to interleukin-4 and -13 (IL4/IL13) has incurred interest for their reparative properties. Unexpectedly, while macrophages exposed to the classic pro-inflammatory signals (interferon-γ/lipopolysaccharide, IFN/LPS) killed neurons and oligodendrocytes in culture, the addition of LPS to IL4/IL13-treated macrophages profoundly elevated IL10, repair metabolites (lactate, ornithine), glucose metabolism and the oligodendrocyte-trophic heparin-binding epidermal growth factor (HBEGF); cells did not display pro-inflammatory or neurotoxic features. In mice with spinal cord demyelination, locally-applied IL4/IL13 was insufficient to alter responses beyond controls; remarkably, the LPS/IL4/IL13-treated animals significantly increased lesional phagocytic macrophages/microglia, lactate and HBEGF levels, oligodendrogenesis and remyelination. We report a remarkably reparative state of macrophages that is unexpectedly generated by the integration of pro- (LPS) and anti- (IL4/IL13) inflammatory activation cues.

2019-09-06 | PXD015021 | Pride

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