Human peripheral IL-10-secreting vs non- IL-10-secreting B cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE35002 | GEO | 2013/03/04
SECONDARY ACCESSION(S): PRJNA151071
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional profiling of human peripheral B cell subsets sorted by flow cytometry based on the secretion of IL-10 in response to CpG2006 stimulation. Goal was to identify molecular markers to distinguish IL-10-producing B cells form non-IL-10-producing B cells. Two-condition experiment, non-IL-10-secreting B cells vs. IL-10-secreting B cells. Healthy donors. Biological replicates: 6
2013-03-04 | E-GEOD-35002 | biostudies-arrayexpress
Project description:The mechanisms in regulating the development of IL-10 producing B cells are largely unknown. To clarify which transcription factor is critical for regulation of IL-10 producing B cells, we compared the gene expression profile of IL-10 positive B cells and IL-10 negative B cells. Transcriptional repressor Prdm1/Blimp1 is known to play a key role in controlling B ells differentiation. We show a dual role for Blimp-1 in IL-10 expression in IL-10 producing B cells and plasmablasts.
2019-09-11 | GSE129260 | GEO
Project description:Following combined stimulation through Toll-like receptor (TLR)-9 and the B-cell receptor (BCR), human B cells were sorted based on IL-10 expression. Microarray analysis showed that just ~0.7% of genes were differentially expressed between IL-10- and IL-10+ B-cells. However, connectivity map analysis revelaed that the IL-10+ cells were those undergoing differentiation to germincal centre B cells, and we identified a CD11c- B-cell subset that was enriched in cells capable of producing IL-10 B-cells were isolated using the Dynabeads Untouched Human B-cells kit, stimulated during 48 hours and then sorted based on IL-10 using secretion assay kit and cell sorter.
2014-06-25 | E-GEOD-50895 | biostudies-arrayexpress
Project description:Microglia, the resident macrophages of the brain parenchyma, are central players in CNS development, homeostasis and disorders. Distinct brain pathologies seem associated with discrete microglia activation modules. How microglia regain their ground state following challenges remains much less understood. Here, we explored the role of the IL-10 axis in restoring murine microglia homeostasis following peripheral endotoxin challenge. Specifically, we show that lipopolysaccharide (LPS)-challenged mice harboring IL-10 receptor-deficient microglia display neuronal impairment and succumb to fatal sickness. Addition of a microglial TNF deficiency rescues these animals, suggesting a microglia-based circuit driving pathology. Single cell transcriptome analysis revealed various IL-10 producing resident and recruited immune cell in the CNS, including most prominently Ly49D+ NK cells and neutrophils, but not microglia. Collectively, we define the kinetics of the microglia response to peripheral endotoxin challenge, including their activation and robust silencing, and highlight the critical role of non-microglial IL-10 in preventing deleterious microglia hyperactivation.
2020-10-22 | GSE157480 | 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 | GSE121267 | 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 | 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 | GSE121284 | GEO
Project description:In the present study we describe a new subset of murine T cells producing high levels of IL-10 that, in this case, are induced by C-type lectin receptor-stimulated (i.e., Dectin-1-stimulated) dendritic cells. This T cell produces IL-10 as a result of a transcriptional mechanism that is distinct from that inducing IL-10 in Th2 cells, Tr1 cells or other T cell subsets. In particular, the mechanism involves mTOR signaling and induction of the LIP isoform of C/EBPb, a factor that interacts with phospho-CREB and GATA3 to induce transactivation of the IL-10 gene. These T cells have strong regulatory properties in relation to fungal infection and hence have been termed Tr2 regulatory T cells to distinguish them from other regulatory T cell subsets.
2017-10-14 | GSE87673 | GEO