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Follicular dendritic cells restrict IL4 availability in germinal centers and foster memory B cell generation

ABSTRACT: Follicular dendritic cells restrict IL4 availability in germinal centers and foster memory B cell generation

PROVIDER: PRJNA750102 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15264072.fastq.gz	Fastqsanger.gz
	SRR15264073.fastq.gz	Fastqsanger.gz
	SRR15264074.fastq.gz	Fastqsanger.gz
	SRR15264075.fastq.gz	Fastqsanger.gz
	SRR15264076.fastq.gz	Fastqsanger.gz

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Follicular dendritic cells restrict IL4 availability in germinal centers and foster memory B cell generation

Project description:Germinal centers (GCs) are sites of antibody affinity maturation and memory B cell generation. Follicular dendritic cells (FDCs) form a dense stromal network within GCs, but the full extent of their supportive activity is not understood. Here we showed that FDCs expressed IL4Ra and they reduced IL4 availability in GCs. We used scRNA-seq to examine IL4 actions within the GC and identified a subset of light zone cells marked by high IL4Ra and CD23 and lack of a Myc gene-expression signature. Trajectory inference analysis suggested this population could differentiate into pre-memory and pre-plasma cells. Genetic experiments showed that IL4Ra and STAT6 acted intrinsically to restrain pre-memory B cell generation. By reducing IL4 availability, FDCs enhanced GC B cell selection and fostered memory cell generation. This work suggests that GC FDCs provide a niche that limits bystander IL4 activity, focusing IL4 action on B cells undergoing selection and enhancing memory cell differentiation

2021-09-15 | GSE180920 | GEO

Follicular dendritic cells restrict interleukin-4 availability in germinal centers and foster memory B cell generation.

Project description:B cells within germinal centers (GCs) enter cycles of antibody affinity maturation or exit the GC as memory cells or plasma cells. Here, we examined the contribution of interleukin (IL)-4 on B cell fate decisions in the GC. Single-cell RNA-sequencing identified a subset of light zone GC B cells expressing high IL-4 receptor-a (IL4Ra) and CD23 and lacking a Myc-associated signature. These cells could differentiate into pre-memory cells. B cell-specific deletion of IL4Ra or STAT6 favored the pre-memory cell trajectory, and provision of exogenous IL-4 in a wild-type context reduced pre-memory cell frequencies. IL-4 acted during antigen-specific interactions but also influenced bystander cells. Deletion of IL4Ra from follicular dendritic cells (FDCs) increased the availability of IL-4 in the GC, impaired the selection of affinity-matured B cells, and reduced memory cell generation. We propose that GC FDCs establish a niche that limits bystander IL-4 activity, focusing IL-4 action on B cells undergoing selection and enhancing memory cell differentiation.

| S-EPMC8516727 | biostudies-literature

Alcanivorax sp. IL4

Project description:Alcanivorax sp. IL4 Genome sequencing

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Emodin inhibits macrophage alernative activation [Control-IL4-Emodin]

Project description:In order to fully characterize emodin's effects on macrophage alternative activation, peritoneal macrophages were stimulated with IL4 with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IL4 induced changes in a large percentage of genes (60%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M2 macrophage activation including: Arg1, Chi3l3, and CD206. Three-condition, one-color experiment: Vehicle control, IL4 or IL4-Emodin treated periferal WBC PMN samples: 4 biological replicates each.

2016-07-04 | E-GEOD-73309 | biostudies-arrayexpress

B cell response to CD40 and IL4 treatment

Project description:Temporal analysis (60, 180, 360 min) of B cells treated with CD40 alone, IL4 alone or CD40 and IL4 (all in triplicates). Keywords: other

2004-02-13 | GSE1023 | 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

Next Generation Sequencing reveals different transcriptome induced by IL4-10 fusion protein (IL4-10 FP) compared to the combination of cytokines in mice with inflammatory pain

Project description:Purpose: The goalsof this study was to compare the transcriptome profiling of dorsal root ganglia (DRG) of animals injected intrathecally with IL4-10 FP, the combination of IL4+IL10 or vehicle, one week after induction of persistent inflammatory pain. Methods: Mice received an intraplantar injection of carrageenan and one week developing inflammatory pain were intrathecally injected with IL4-10 FP, IL4+IL10 or PBS. DRGs were isolated and RNA libraries were prepared with the poly A selection method followed by multiplexing and sequencing on the Illumina NextSeq500® platform in a 1 × 75bp single-read and 350 million reads per lane (Utrecht Sequencing Facility) Results: In vivo IL4-10 FP induces a differential transcriptome than the combination of cytokines in mice with persistent inflammatory pain. Conclusions: The superior analgesic effect observed in mice treated with IL4-10 FP compared to mice injected with the naïve cytokines is derived from an induction of a different transcriptome on the lumbar DRGs.

2021-02-28 | GSE150795 | GEO

Expression data from 5 rhesus tissues at 3 centers

Project description:Novel approaches were used to generate the DNA sequence information for the rhesus GeneChip (2005). The purpose of this experiment was to test its reliability and validity of the rhesus macaque GeneChip across different tissues and centers. Keywords: reliability To test the reliability of the rhesus GeneChip across different centers, RNA was isolated from five sources: cerebral cortex, pancreas, thymus, testis, and an immortalized fibroblast cell line. Aliquots of this RNA were sent to each of three centers: Yerkes National Primate Research Center, Oregon National Primate Research Center and the University of Nebraska Medical Center. Each center labeled the samples and hybridized them to two rhesus macaque GeneChips.

2010-06-11 | E-GEOD-7094 | biostudies-arrayexpress

Emodin inhibits macrophage alernative activation [Control-IL4-Emodin]

2016-01-02 | GSE73309 | GEO

Mutant p53 regulates survivin to foster lung metastasis

Project description:Mutant p53 regulates survivin to foster lung metastasis

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